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Principles of interleukin (IL)-6-type cytokine signalling and its regulation
Open accessAbstract
The IL (interleukin)-6-type cytokines IL-6, IL-11, LIF (leukaemia inhibitory factor), OSM (oncostatin M), ciliary neurotrophic factor, cardiotrophin-1 and cardiotrophin-like cytokine are an important family of mediators involved in the regulation of the acute-phase response to injury and infection. Besides their functions in inflammation and the immune response, these cytokines play also a crucial role in haematopoiesis, liver and neuronal regeneration, embryonal development and fertility. Dysregulation of IL-6-type cytokine signalling contributes to the onset and maintenance of several diseases, such as rheumatoid arthritis, inflammatory bowel disease, osteoporosis, multiple sclerosis and various types of cancer (e.g. multiple myeloma and prostate cancer). IL-6-type cytokines exert their action via the signal transducers gp (glycoprotein) 130, LIF receptor and OSM receptor leading to the activation of the JAK/STAT (Janus kinase/signal transducer and activator of transcription) and MAPK (mitogen-activated protein kinase) cascades. This review focuses on recent progress in the understanding of the molecular mechanisms of IL-6-type cytokine signal transduction. Emphasis is put on the termination and modulation of the JAK/STAT signalling pathway mediated by tyrosine phosphatases, the SOCS (suppressor of cytokine signalling) feedback inhibitors and PIAS (protein inhibitor of activated STAT) proteins. Also the cross-talk between the JAK/STAT pathway with other signalling cascades is discussed.
Overview
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Written from the paper’s full text.
TL;DR
This review summarizes IL-6-type cytokine signalling through gp130, LIFR and OSMR, covering JAK/STAT and MAPK activation and the mechanisms that terminate or modulate these pathways. It emphasizes negative regulation by tyrosine phosphatases, SOCS feedback inhibitors and PIAS proteins, as well as cross-talk with other signalling cascades.
Key findings
- IL-6-type cytokines (IL-6, IL-11, LIF, OSM, CNTF, CT-1 and CLC) signal via gp130 homodimers or gp130–LIFR/OSMR heterodimers; all potently activate STAT3 and, to a lesser extent, STAT1 through gp130, while OSMR is the most potent activator of STAT5.
- Receptor activation requires more than simple dimerization: efficient gp130 activation by monoclonal antibodies required two distinct antibodies, with the minimal requirement being one intact antibody plus the Fab of a second; insertion of one to four alanines into the gp130 membrane-proximal intracellular region gave full activation only with wild-type and the +3A mutant, interpreted as an approx. 110° twist per alanine and approx. 330° for three.
- JAK1 is essential for IL-6 signalling; gp130, LIFR and OSMR bind JAK1, JAK2 and TYK2. JAK1 mobility is approx. 100-fold lower than that of a typical cytoplasmic protein, and gp130 residues including box1 prolines and Trp666 are critical for JAK binding, while W652A abrogates JAK1 activation without affecting JAK1 association.
- Signal termination involves SHP2 and SOCS3 at gp130 pTyr759, with SOCS3 binding gp130 peptides with slightly higher affinity than SHP2; SOCS1 and SOCS3 inhibit JAKs, PIAS1 inhibits STAT1 and PIAS3 inhibits STAT3. Reported half-lives include SOCS1 1.5 h, SOCS2 1 h, SOCS3 1.6 h, IL-6Rα 2–3 h, gp130 2.5 h, JAK1 3.2 h, JAK2 1.9 h, TYK2 2 h, STAT3α 8.5 h, STAT3β 4.5 h, STAT1 16 h and SHP-2 18–20 h.
Methods
- Narrative review of molecular mechanisms of IL-6-type cytokine signal transduction, focusing on advances made during the previous 5 years in receptor activation, JAK–receptor interactions, STAT activation, signal modulation and cross-talk.
- Synthesizes structural, mutagenesis, biochemical and in vivo findings from the literature; no primary experimental dataset is presented, and the text includes models and a table of half-lives drawn from cited studies.
Limitations
- The authors state that key structural data are still missing, including the structure and conformational states of the cytoplasmic parts of cytokine receptors, and that three-dimensional structures of JAKs and SOCS proteins would be extremely valuable.
- The authors state that mathematical models of this complexity suffer from a lack of sufficient quantitative experimental data, and that cross-talk and biological outcomes depend on cell type and differentiation state.
- Evident from the text: as a narrative review, it does not use a systematic search or meta-analysis, and it includes unpublished work/personal communications and unresolved conflicting findings, such as JNK versus p38 involvement in STAT3 Ser727 phosphorylation and the positive versus negative regulatory functions reported for STAT3β.
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Claims the paper makes
172 Sources not found · 17 Own interpretation · 16 No basis given · 7 Not checked yet · 2 Own result
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In the paper
“Human OSM has the exceptional capability to recruit two different receptor complexes.It forms both LIFR-gp130 and OSMR-gp130 heterodimers.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“LIF and OSM directly engage their signalling receptor subunits without requirement for additional α-receptor subunits (Figure 2) [4,6].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“Soluble forms of cytokine receptors in vivo are formed either by limited proteolysis (shedding) of membrane-bound receptors or by translation from an alternatively spliced mRNA [4].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“It has been demonstrated that sIL-6Rα potentiates the antagonistic activity of sgp130.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“In contrast with IL-6, and presumably also IL-11, where all the helices are straight, the A helix of LIF, OSM and CNTF is kinked [17,18].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“The minimal requirement for receptor activation is one intact antibody and the Fab (fragment antigen binding) of the second antibody.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptors at work: let's do the twist
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In the paper
“It has been shown that these domains are necessary for coupling ligand binding and signal transduction, since deletion of these domains leads to signalling incompetent receptors [36,37].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptors at work: let's do the twist
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“Thus in the homodimer two different binding epitopes of gp130 are involved in ligand recognition [23].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“The interaction sites predicted by mutagenesis studies have recently been confirmed by the X-ray structure of KSHV-IL-6 bound to a soluble gp130 fragment comprising the CBM and the Ig-like domain [24].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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“In contrast with the α-receptors, the receptors that initiate signal transduction have three additional membrane-proximal FNIII domains [4].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“This structural divergence might reflect differences in the mechanisms of receptor recruitment, since the straight cytokines signal via gp130 homodimers, whereas the kinked cytokines signal via LIFR-gp130 or OSMR-gp130 heterodimers.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“Of these, JAK1 plays an essential role, because in cells lacking JAK1 IL-6 signal transduction is greatly impaired [51,52,134].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptor-JAK interaction: more than just a rendez-vous
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In the paper
“This finding has been interpreted in a way that the bivalent intact antibody enforces receptor dimerization and the monovalent Fab adjusts the conformation required for JAK activation and downstream signalling [40].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptors at work: let's do the twist
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In the paper
“Some evidence has been provided that under certain circumstances gp130 and LIFR are degraded after internalization [30][31][32].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“While for gp130, the STATs were found to depend on a specific conformation in order to become phosphorylated, for the EpoR the receptor phosphorylation seems to be sensitive to changes in orientation.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptors at work: let's do the twist
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In the paper
“KSHV-IL-6 binds the gp130 homodimer in the absence of any α-receptor [16], but with lower affinity as compared with IL-6-IL-6Rα-gp130 ternary complexes.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“Internalization of gp130 seems to be independent from ligand binding [28], and is modulated by phosphorylation at Ser 782 [29] which is located adjacent to the dileucine motif.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“ErbB2 forms a complex with gp130 in an IL-6-dependent manner in prostate carcinoma cells [35].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“In certain cell types, a localization of gp130 in plasma membrane microdomains, such as lipid rafts and caveolae, has been observed [9][10][11].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“After secretion of the CLC-CLF-1 or CLC-CNTFRα complexes, signalling is dependent on CNTFRα and occurs via gp130-LIFR heterodimers.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > INTRODUCTION
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In the paper
“Constantinescu et al. [46] identified a hydrophobic motif in the EpoR membrane-proximal domain (Leu 253 , Ile 257 and Trp 258 ) which is conserved in many cytokine receptors and needs to be precisely orientated in order to promote signalling.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptors at work: let's do the twist
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In the paper
“PKCδ enhances the association of STAT3 with the receptor, which possibly involves the phosphorylation of Thr 890 of gp130 [67].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptor-JAK interaction: more than just a rendez-vous
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In the paper
“All IL-6-type cytokines potently activate STAT3, and to a minor extent STAT1 through their common receptor subunit gp130 [4].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Another face of JAKs: determination of the receptor's fate
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In the paper
“The Cterminal tyrosine kinase domain is preceded by a pseudokinase domain, which itself is devoid of catalytic activity, but regulates the activity of the kinase domain [3].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptor-JAK interaction: more than just a rendez-vous
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In the paper
“In the cases of LIFR and OSMR, STAT3 and STAT1, as well as STAT5, activation has been observed, with OSMR being the most potent activator of STAT5 [56].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Another face of JAKs: determination of the receptor's fate
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In the paper
“These results were confirmed by Chung et al. [105], who also observed that IL-6-induced STAT3 activation is MAPK independent, but sensitive to H7.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Serine phosphorylation
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In the paper
“Cdk9 (cyclin-dependent kinase 9) was also found to bind to gp130, and the association increased upon IL-6 stimulation of HEK 293 cells over-expressing gp130 and Cdk9 [66].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptor-JAK interaction: more than just a rendez-vous
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In the paper
“Deletion of these amino acids reduces IL-6-induced Hck kinase activity, ERK (extracellular-regulated kinase) activation, dephosphorylation of Pyk2 and proliferation of transfected pro-B Ba/F3 cells [65].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptor-JAK interaction: more than just a rendez-vous
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In the paper
“A conformational change in the SH2 domain may account for this dual specificity [91].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Another face of JAKs: determination of the receptor's fate
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In the paper
“The recruitment of STATs to the activated receptors has been shown to be mediated by their SH2 domain and requires the phosphorylation of receptor tyrosine motifs [74,[81][82][83].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Another face of JAKs: determination of the receptor's fate
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In the paper
“substitution of Trp 652 with alanine (W652A) within the box1 region has no effect on JAK1 association but abrogates JAK1 activation.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptor-JAK interaction: more than just a rendez-vous
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Mutations with similar consequences (no JAK activation in spite of JAK association) have been described for the EpoR [59], indicating that cytokine receptors in general contribute to the JAK-activation process.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptor-JAK interaction: more than just a rendez-vous
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Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“human fibrosarcoma cells lacking JAK1 express less OSMR at their surface compared with the parental cells, but transient transfection of JAK1 can again increase the amount of surface-expressed receptors [49].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Another face of JAKs: determination of the receptor's fate
What the sources say
- Not matchedcites [49]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“Box2 of gp130, a sequence dominated by hydrophobic amino acids followed by charged ones, contributes to JAK binding, presumably by increasing the affinity; a gp130 construct lacking box2 coprecipitates with JAK1 only when the kinase is over-expressed [55].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Receptor-JAK interaction: more than just a rendez-vous
What the sources say
- Not matchedcites [55]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“This leads to the formation of active STAT dimers, also shown to be mediated by their SH2 domains [90].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Another face of JAKs: determination of the receptor's fate
What the sources say
- Not matchedcites [90]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In response to IL-6, Gab1 is tyrosine phosphorylated and interacts subsequently with SHP2 and PI3K.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of MAPK cascades: one tyrosine to make things more complicated
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A recent study [112] on STAT3 activation in response to EGF (epidermal growth factor) suggests that receptor-mediated endocytosis is required for shuttling of STAT3 from the plasma membrane to the perinuclear region.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT nuclear translocation: not a one way ticket
What the sources say
- Not matchedcites [112]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“In the DNA-binding domain of STAT1, initially an NES was postulated that comprises residues 399-410 [108].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT nuclear translocation: not a one way ticket
What the sources say
- Not matchedcites [108]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“Compared with the unmethylated protein, methylated STAT1 has a higher tendency to associate with DNA, since its interaction with PIAS (protein inhibitor of activated STATs) 1 (see the subsection below entitled 'PIAS -more than inhibitors of activated STATs?') seems to be weaker [106].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Methylation of STATs
What the sources say
- Not matchedcites [106]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“The family of IL-6-type cytokines not only activates ERK1/2, a MAPK known for cellular processes that maintain cell survival, but also the stress-activated members of the MAPK family: p38 and JNK [140-142] (Figure 6).”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of MAPK cascades: one tyrosine to make things more complicated
What the sources say
- Not matchedcites [140]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [141]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [142]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Sensitivity to leptomycin suggests that nuclear export of STAT1 involves the nuclear export receptor CRM-1 that also acts in a Randependent manner [108,109].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT nuclear translocation: not a one way ticket
What the sources say
- Not matchedcites [108]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [109]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“However, from an earlier study [113], it was concluded that nuclear translocation of STAT1 in response to IFNγ does not require cytoskeletal structures, such as actin filaments or microtubules.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT nuclear translocation: not a one way ticket
What the sources say
- Not matchedcites [113]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“According to the current view of the SHP2-dependent activation of MAPKs adopted from EGF and PDGF (platelet-derived growth factor) signal transduction, SHP2 links the Grb2-SOS (growthfactor-receptor-bound protein/Son of Sevenless) complex and/or Gab1 (Grb2-associated binder-1) to gp130 [127,129,130].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of MAPK cascades: one tyrosine to make things more complicated
What the sources say
- Not matchedcites [127]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [129]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [130]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“In response to IL-2, Epo, EGF, and PDGF, SOCS3 (suppressor of cytokine signalling 3) becomes tyrosine phosphorylated, and subsequently binds and inactivates Ras/GTPase-activating protein.This results in the inhibition of the GTPase activity of Ras, leading to a sustained Ras/GTP and MAPK activity [139].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of MAPK cascades: one tyrosine to make things more complicated
What the sources say
- Not matchedcites [139]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“SHP2 is rapidly recruited to tyrosine-phosphorylated gp130 and becomes also phosphorylated in a JAK1-dependent manner [131].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of MAPK cascades: one tyrosine to make things more complicated
What the sources say
- Not matchedcites [131]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Dimerization of IL-6-type cytokine receptors does not only lead to activation of the JAK/STAT-signalling pathway, but also to the induction of the MAPK cascade.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of MAPK cascades: one tyrosine to make things more complicated
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Furthermore, nuclear accumulation of constitutively active STAT proteins is independent from endocytosis, because in these cases the STATs are not recruited to any plasma membrane receptor [110,114].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT nuclear translocation: not a one way ticket
What the sources say
- Not matchedcites [110]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [114]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“PIAS1 inhibits STAT1 signalling [179], but conversely enhances the transcriptional activity of nuclear hormone receptors [180].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > PIAS -more than inhibitors of activated STATs?
What the sources say
- Not matchedcites [179]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [180]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Whereas SHP2 modulates the amount and amplitude of STAT3 activity [131,158], PTPεC affects the kinetics of the onset of STAT3 activation [169].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Protein tyrosine phosphatases (PTPs): what goes up must come down
What the sources say
- Not matchedcites [131]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [158]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [169]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“It should be noted, however, that PI3K activation upon IL-6 treatment is observed in a cell-type specific manner; e.g.no significant Akt activation could be observed in IL-6treated HepG2 hepatoma cells [149].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of the PI3K cascade: the lipid connection
What the sources say
- Not matchedcites [149]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“This enzyme modifies certain phosphatidylinositides, so that the serine/threonine kinase protein kinase B/Akt is recruited to the plasma membrane, where it becomes activated through phosphorylation by PDK1 (phosphoinositide-dependent kinase-1).”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of the PI3K cascade: the lipid connection
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Early results suggested the presence of a nuclear phosphatase which counteracts IFNγ -activated STAT1 and contributes to its nuclear export [121,173].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Protein tyrosine phosphatases (PTPs): what goes up must come down
What the sources say
- Not matchedcites [121]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [173]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Interaction of SHP2 with JAK1, JAK2 and TYK2, and phosphorylation of SHP2 by JAK1 and JAK2, have at least been shown to occur in vitro [131,162].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Protein tyrosine phosphatases (PTPs): what goes up must come down
What the sources say
- Not matchedcites [131]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [162]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“IL-6-induced activation of the PI3K/Akt pathway is involved in protection against apoptosis, as well as in enhanced proliferation of multiple myeloma cells [145][146][147].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Activation of the PI3K cascade: the lipid connection
What the sources say
- Not matchedcites [145]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [146]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [147]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“The cytoplasmic variant of PTPε, PTPεC, is expressed in haematopoietic cells and has been shown to selectively inhibit IL-6-induced gp130, JAK and STAT activation [168].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Protein tyrosine phosphatases (PTPs): what goes up must come down
What the sources say
- Not matchedcites [168]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“On the other hand, the IL-6induced activation of the MAPK cascade is impaired by mutation of Tyr 759 within gp130, indicating that SHP2, as an adaptor, has a positive function on the activation of the MAPK cascade (as shown in Figure 1).”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Protein tyrosine phosphatases (PTPs): what goes up must come down
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The family of PIAS comprises five mammalian members: PIAS1, PIAS3, PIASxα, PIASxβ, and PIASy.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > PIAS -more than inhibitors of activated STATs?
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus methylation not only supports STAT activity (by preventing PIAS association), but also promotes its inactivation by dephosphorylation.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Protein tyrosine phosphatases (PTPs): what goes up must come down
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Experiments in vivo underscore the in vitro findings in demonstrating that mice expressing gp130 lacking Tyr 759 display splenomegaly, lymphadenopathy and an enhanced acute-phase reaction [161].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Protein tyrosine phosphatases (PTPs): what goes up must come down
What the sources say
- Not matchedcites [161]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These differences suggest that signalling components requiring posttranslational modifications for their activation are long-lived, whereas the activity of short-lived proteins is regulated mainly at the transcriptional level.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Half-lives of signalling components: party as long as you live
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Whereas the feedback inhibitors SOCS1, SOCS2 and SOCS3 are very short-lived, STAT1, STAT3α and SHP2 have slow turnover rates.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > Half-lives of signalling components: party as long as you live
What the sources say
- Not matchedcites [222]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [223]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The eight members of this family (CIS and SOCS1-SOCS7) contain a central SH2 domain, as well as a C-terminal domain called a SOCS box (Figure 4).”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > The SOCS family of feedback inhibitors: natural born terminators
plainn = 8- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“For gp130, SOCS3 has been found to bind to the phosphotyrosine motif 759 [197,198], which is also the binding site for SHP2.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > The SOCS family of feedback inhibitors: natural born terminators
What the sources say
- Not matchedcites [197]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [198]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“Phosphorylation occurs at two tyrosine residues (Tyr 204 and Tyr 221 ) within the SOCS box and phosphorylation of Tyr 221 recruits p120 RasGAP leading to sustained ERK activation [139].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > The SOCS family of feedback inhibitors: natural born terminators
What the sources say
- Not matchedcites [139]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Other reports, however, suggest that elongin C binding can stabilize SOCS1 and that the disruption of the interaction leads to proteasomal degradation of SOCS1 [206,215].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > The SOCS family of feedback inhibitors: natural born terminators
What the sources say
- Not matchedcites [206]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [215]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Expression of SOCS proteins was found to be rapidly up-regulated by IL-6 (CIS, SOCS1, SOCS2 and SOCS3), LIF (CIS, SOCS1, SOCS2 and SOCS3), IL-11 (SOCS3) and OSM (CIS, SOCS1 and SOCS3) [32,190,192,193].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > The SOCS family of feedback inhibitors: natural born terminators
What the sources say
- Not matchedcites [32]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [190]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [192]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As SOCS proteins are induced via the JAK/STAT pathway and subsequently inhibit STAT-mediated signal transduction, they are acting as classical feedback inhibitors.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > The SOCS family of feedback inhibitors: natural born terminators
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“These phosphotyrosine residues may be part of an activated receptor or the tyrosine-phosphorylated C-terminal tail of SHP2 (from [156]).”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > PERSPECTIVES
What the sources say
- Not matchedcites [156]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“FKHR specifically enhanced the activity of STAT3-dependent promoters, such as the α 2 M promoter, but not that of a STAT5-responsive promoter.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT action within the transcriptosome: where transcription factors gather
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Other signalling pathways have been shown to induce stabilization of cytokine mRNAs as well: the JNK pathway induces stabilization of the short-lived IL-2 mRNA [219], and PI3K activation induces stabilization of IL-3 mRNA [220].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > PERSPECTIVES
What the sources say
- Not matchedcites [219]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [220]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“PI3K activation induces stabilization of IL-3 mRNA [220]”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > PERSPECTIVES
What the sources say
- Not matchedcites [220]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“The nuclear receptor co-repressor SMRT (silencing mediator of retinoic and thyroid hormone receptors) is a potential binding partner for STAT5 and represses STAT5-dependent transcription [255].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT action within the transcriptosome: where transcription factors gather
What the sources say
- Not matchedcites [255]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“Furthermore, FKHR and STAT3 can be co-immunoprecipitated and co-localize in the nucleus of IL-6-treated HepG2 cells [149].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT action within the transcriptosome: where transcription factors gather
What the sources say
- Not matchedcites [149]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“the JNK pathway induces stabilization of the short-lived IL-2 mRNA [219]”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > PERSPECTIVES
What the sources say
- Not matchedcites [219]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Interestingly, an EZI mutant predominantly localized in the cytoplasm inhibited nuclear localization of STAT3, as well as STAT3-mediated transactivation.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT action within the transcriptosome: where transcription factors gather
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Interestingly, Nmi itself is induced by IL-2 and IFNγ , indicating a positive feedback loop within this signal transduction.”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT action within the transcriptosome: where transcription factors gather
What the sources say
- Not matchedcites [253]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“This interaction is further modulated by Nmi (N-Myc interactor) which augments CBP recruitment to STAT1 and STAT5, and potentiates IL-2 and IFNγ signalling [253].”
§ Principles of interleukin (IL)-6-type cytokine signalling and its regulation 1 > STAT action within the transcriptosome: where transcription factors gather
What the sources say
- Not matchedcites [253]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The authors state this as an assumption.
The membrane-proximal FNIII domains bridge the ~9 nm distance between the CBM C-termini so that the cytoplasmic parts are close enough to become activated by associated JAKs.
“The membrane-proximal FNIII domains might bridge this distance so that the cytoplasmic parts are in close enough proximity to become activated by the associated JAKs (Figure 5).This assumption is supported by a recent study on the role of the gp130 FNIII domains for heterodimerization with the LIFR [38].”
The paper relies on this without support.
gp130 is ubiquitously expressed.
“Although gp130 is ubiquitously expressed, the number of cells that respond to a certain IL-6-type cytokine is limited, since the expression of the other receptor subunits, especially of the α-receptors, is more restricted and tightly regulated.”
The paper relies on this without support.
IL-6-type cytokines form a subfamily of helix bundle cytokines.
“IL-6-type cytokines form a subfamily of the helix bundle cytokines.”
The paper relies on this without support.
All IL-6-type cytokines comprise four long α-helices A-D arranged in an up-up-down-down topology.
“All IL-6-type cytokines comprise four long α-helices termed A, B, C and D, which are arranged in a way that leads to an up-up-down-down topology (Figure 3).”
The paper relies on this without support.
Each receptor contains at least one cytokine-binding module (CBM) comprising two FNIII domains.
“Each receptor contains at least one cytokine-binding module (CBM) that comprises two FNIII-domains.”
The paper relies on this without support.
JAKs bind to the membrane-proximal region of cytokine receptors, which contains conserved box1 and box2 motifs.
“JAKs bind to the membrane-proximal region of cytokine receptors, which contains conserved so-called box1 and box2 motifs.”
The paper relies on this without support.
The N-terminal region of JAKs comprises a FERM domain crucial for receptor association.
“The N-terminal region of JAKs comprises a FERM (fourpoint-one, ezrin, radixin and moesin) domain which is crucial for receptor association.”
The paper relies on this without support.
The STAT family encompasses seven mammalian members.
“The STAT family of transcription factors encompasses seven mammalian members, designated STAT1, -2, -3, -4, -5a, -5b and -6.”
The paper relies on this without support.
In response to IL-6 stimulation, cytoplasmic STAT3 rapidly accumulates in the nucleus.
“In response to IL-6 stimulation, cytoplasmic STAT3 rapidly accumulates in the nucleus.”
The paper relies on this without support.
Nuclear accumulation is triggered by STAT dimerization in response to tyrosine phosphorylation.
“Nuclear accumulation is triggered by STAT dimerization in response to tyrosine phosphorylation.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“IL-6Rα expression is normally associated with hepatocytes and leukocytes but has also been described in cancer cells, including PDAC.”
From Dynamic IL-6R/STAT3 signaling leads to heterogeneity of metabolic phenotype in pancreatic ductal adenocarcinoma cells (2024) · cites this paper as [40]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The cytokine IL-6 triggers multiple downstream responses, including metabolic regulation.”
From Dynamic IL-6R/STAT3 signaling leads to heterogeneity of metabolic phenotype in pancreatic ductal adenocarcinoma cells (2024) · cites this paper as [40]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“IL-6, which was discovered in 1986 (27), is a pleiotropic cytokine involved not only in immune responses but also in inflammation, hematopoiesis, bone metabolism, embryonic development and other fundamental processes (1, 21, 28–32).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [30]
Experimental — accuracy not yet measured
Citations
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Structure and function of a new STAT-induced STAT inhibitor
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Specific Inhibition of Stat3 Signal Transduction by PIAS3
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Cited by
Sorted by citations
Items 2,001–2,100 of 3,269
Inhibitory Mechanism of the Outer Membrane Growth of Chronic Subdural Hematomas
Osuka, K., Watanabe, Y., Usuda, N., Aoyama, M., Iwami, K., Takeuchi, M., Watabe, T., & Takayasu, M. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2016.4623 · Cited by 13
“6,11 14 However, the regulatory mechanisms of the IL-6/gp130/JAK/STAT3 signaling pathway in the outer membrane of CSDHs have not been clarified.”
Neuroprotective effect of secreted factors from human adipose stem cells in a rat stroke model
Seo, H. G., Yi, Y., Oh, B., & Paik, N. (2017) · Neurological Research · doi:10.1080/01616412.2017.1379293 · Cited by 14
Liu, X., Heitz, P., Roux, M. J., Keller, D., Bourcier, T., Sauer, A., Prévost, G., & Gaucher, D. (2018) · Scientific Reports · doi:10.1038/s41598-018-20590-z · Cited by 13
“IL-6 interacts with its receptor and then elicits JAK/STAT (Janus kinase/signal transducer and activator of transcription) and MAPK (mitogen-activated protein kinase) pathways which enhance numerous biological activities 40 .”
Hügle, B., Schippers, A., Fischer, N., et al. (2018) · Arthritis Research & Therapy · doi:10.1186/s13075-018-1603-2 · Cited by 13
“In contrast, finding STAT3 as the third most prominent transcription factor is unsurprising, since STAT3 signals downstream of IL-6, a well-known therapeutic target using tocilizumab in sJIA [24, 25].”
BackgroundMurray, N. P. (2018) · Biological Research · doi:10.1186/s40659-018-0180-9 · Cited by 13
Die Rolle von Interleukin-11 beim Osteosarkom
Lokau, J., Schoeder, V., & Garbers, C. (2020) · Der Pathologe · doi:10.1007/s00292-020-00756-1 · Cited by 13
Thang, L. V., Duc, L. N., Trung, K. N., Dũng, N. H., Quyen, D. B. Q., Tuan, N. M., Ha, D. M., Kien, T. Q., Dung, N. T. T., Vân, D. T., et al. (2020) · International Urology and Nephrology · doi:10.1007/s11255-020-02461-7 · Cited by 13
“IL-6 is responsible for stimulating acute-phase protein synthesis, as well as the production of neutrophils in bone marrow [1].”
BackgroundLjungberg, L. U., Zegeye, M. M., Kardeby, C., Fälker, K., Repsilber, D., & Sirsjö, A. (2020) · Mediators of Inflammation · doi:10.1155/2020/4623107 · Cited by 13
“IL6 binds to its specific and nonsignaling receptor IL6 receptor α (IL6Rα), which forms a dimeric complex with the signaling-transducing receptor gp130 (IL6ST) which in turn mediates a signal [8].”
BackgroundFritzenwanger, M., Foerster, M., Meusel, K., et al. (2008) · PubMed · Cited by 13
Honke, N., Ohl, K., Wiener, A., Bierwagen, J., Peitz, J., Fiore, S. D., Fischer, R., Wagner, N., Wüller, S., & Tenbrock, K. (2013) · Arthritis & Rheumatology · doi:10.1002/art.38245 · Cited by 13
Osmotic regulation of STAT3 stability in H4IIE rat hepatoma cells
Lornejad‐Schäfer, M. R., Albrecht, U., Poppek, D., Gehrmann, T., Grune, T., Bode, J. G., Häussinger, D., & Schliess, F. (2005) · FEBS Letters · doi:10.1016/j.febslet.2005.09.053 · Cited by 13
Analysis of target genes induced by IL-13 cytotoxin in human glioblastoma cells
Han, J., Yang, L. M., & Puri, R. K. (2005) · Journal of Neuro-Oncology · doi:10.1007/s11060-004-3119-7 · Cited by 13
“These genes belong to the cell adhesion [40], cell motility [41], DNA repair [42], angiogenesis [43], and signal and metabolic functions [44–46].”
BackgroundLehmann, U., Sommer, U., Smyczek, T., Hörtner, M., Frisch, W., Volkmer‐Engert, R., Heinrich, P., Schaper, F., & Haan, S. (2006) · Cellular Signalling · doi:10.1016/j.cellsig.2005.03.019 · Cited by 19
Self-citationIdentification, characterization and expression of a novel cytokine M17 homologue (MSH) in fish
Hwang, J. Y., Santos, M. D., Kondo, H., et al. (2007) · Fish & Shellfish Immunology · doi:10.1016/j.fsi.2007.06.009 · Cited by 13
“These cytokines have the same four a-helix bundle motif and share a common signal transducing receptor component, glycoprotein 130 (gp130) [1,2].”
BackgroundInterleukin-6 as an early marker for fat embolism
Yoga, R., Theis, J. C., Walton, M., et al. (2009) · Journal of Orthopaedic Surgery and Research · doi:10.1186/1749-799x-4-18 · Cited by 13
“IL-6 is one of the most important cytokine in the acute inflammatory phase [11].”
BackgroundKim, H., Lee, H., & Shin, K. (2016) · Bioscience Biotechnology and Biochemistry · doi:10.1080/09168451.2016.1217149 · Cited by 13
Anti-Inflammatory Actions of Vitamin K
Hodges, S. J., Pitsillides, A. A., Ytrebø, L. M., et al. (2017) · InTech eBooks · doi:10.5772/63891 · Cited by 13
“This feedback is achieved via interaction with its own specific cell surface receptor that activates the Janus kinase (JAK) signal transducer and activator of transcription 3 (STAT3) pathway [55].”
BackgroundKatkam, S. K., Rajasekhar, L., Kumaraswami, K., & Kutala, V. K. (2017) · Lupus · doi:10.1177/0961203317711010 · Cited by 13
Dziemidowicz, M., Bonda, T. A., Литвинович, С. Н., Taranta, A., Winnicka, M. M., & Kamiński, K. A. (2019) · Archives of Medical Science · doi:10.5114/aoms.2019.89452 · Cited by 13
“Phosphorylation of Y757 of the gp130 protein allows for binding the cytoplasmic tyrosine phosphatase Shp2 (protein tyrosine phosphatase – PTP) [19], which further activates Ras protein and subsequently stimulates MAPK (mitogen-activated protein kinases) and PI3K (phosphatidylinositol 3-kinase) cascades [18, 20].”
BackgroundChuang, Y.-H., Chuang, W., Huang, S., Liu, C., & Huang, C. (2009) · Pharmacological Research · doi:10.1016/j.phrs.2009.05.004 · Cited by 13
The prevention and treatment of sepsis: Is interleukin-6 a drug target or a drug?*
Fink, M. P. (2006) · Critical Care Medicine · doi:10.1097/01.ccm.0000203108.60429.df · Cited by 13
C/EBP-δ Induction by gp130 Signaling
Kamaraju, A. K., Adjalley, S. H., Zhang, P., Chebath, J., & Revel, M. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m310443200 · Cited by 13
The biology of interleukin-6 family cytokines is regulated by glycosylation
Kohrs, L., Buettner, F. F. R., Lokau, J., & Garbers, C. (2025) · Biochemical Journal · doi:10.1042/bcj20240769 · Cited by 14
The Molecular Basis and Therapeutic Potential of Leukemia Inhibitory Factor in Cancer Cachexia
Zeng, R., Tong, C., & Xiong, X. (2022) · Cancers · doi:10.3390/cancers14122955 · Cited by 13
“Existing studies have shown that LIFR can be expressed on many cell surfaces, such as on breast epithelial cells, macrophages, adipocytes, liver cells, and muscle [24,35].”
BackgroundUtility of IL-6 in the Diagnosis, Treatment and Prognosis of COVID-19 Patients: A Longitudinal Study
Jain, V., Kumar, P., Panda, P. K., Suresh, M., Kaushal, K., Mirza, A. A., Raina, R., Saha, S., Omar, B. J., & Vivekanandhan, S. (2022) · Vaccines · doi:10.3390/vaccines10111786 · Cited by 12
“COPD CVA CKD CLD Autoimmune disease Malignancy Mean Charlson comorbidity index 12 2 3 2 5 3 2 Severity of Covid-19 at presentation (WHO) Mild Moderate Severe 2 21 108 Severity of Covid-19 at presentation(qCSI score) Low risk (0-3) Low intermediate risk (4-6) High intermediate risk (7-9) High risk (10-12) 32 34 1 0 Res…”
BackgroundLiu, W., Geng, C., Li, X., Li, Y., Song, S., & Wang, C. (2022) · Digestive Diseases and Sciences · doi:10.1007/s10620-022-07805-0 · Cited by 12
“Several tyrosine kinases (Jak1, Jak2, Jak3, and Tyk2) are involved in the regulation of IL-6-STAT3 signaling [24, 25].”
BackgroundMiao, K., & Zhang, L. (2023) · Chinese Medical Journal - Pulmonary and Critical Care Medicine · doi:10.1016/j.pccm.2023.08.002 · Cited by 13
“29 , 30 The Bruton’s tyrosine kinase (BTK) pathway, which is regulated by IL-1, IL-6, and IL-12, plays an important role in the maturation, differentiation, and proliferation of B cells.”
Cytokines of the interleukin-6 family as emerging targets in inflammatory bowel disease
Garbers, C., & Lokau, J. (2024) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2024.2306341 · Cited by 12
Ayub, A., Hasan, M. K., Mahmud, Z., Hossain, M. S., & Kabir, Y. (2024) · Medical Oncology · doi:10.1007/s12032-024-02417-2 · Cited by 13
“NRTK can influence cell proliferation, and cell signaling displayed by NRTK involves the expression control of genes, e.g., via IL-6 transmitted phosphorylation of the membrane-attached TK (Janus kinase), triggering activation of the signal-transducer and activator of transcription (STAT) [106].”
Sun, Y., Tian, Y., Li, Z., Cao, S., Liu, X., Han, H., Han, L., Kong, L., Zhang, X., Liu, F., et al. (2024) · European Journal of Surgical Oncology · doi:10.1016/j.ejso.2024.109563 · Cited by 15
Zorc, R., Redmond, C., Sylvester, M., Maclean, M. J., Almeida, L. Y., Quinn, K. A., Tomelleri, A., Campochiaro, C., Dagna, L., Gutierrez‐Rodrigues, F., et al. (2025) · Annals of the Rheumatic Diseases · doi:10.1016/j.ard.2025.01.049 · Cited by 13
Ruff, K., Puetter, A., & Levy, L. S. (2007) · BMC Cancer · doi:10.1186/1471-2407-7-35 · Cited by 12
“Through this mechanism, IL-6 preferentially activates STAT3 [26].”
BackgroundInfluentialLong-term dynamic profiling of inflammatory mediators in double-hit burn and sepsis animal models
Orman, M. A., Ierapetritou, M., Francois Berthiaume, B., & Androulakis, I. P. (2012) · Cytokine · doi:10.1016/j.cyto.2012.01.017 · Cited by 12
“IL-6 affects signal transducers g130, LIF receptor and OSM receptor leading to activation of the JAK/STAT and MAPK cascades [37].”
BackgroundSagawa, M., Tabayashi, T., Kimura, Y., et al. (2015) · Cancer Science · doi:10.1111/cas.12616 · Cited by 12
Dayoub, R., Buerger, L., Ibrahim, S., Melter, M., & Weiß, T. S. (2017) · Experimental and Molecular Pathology · doi:10.1016/j.yexmp.2017.05.011 · Cited by 12
Winship, A., & Dimitriadis, E. (2017) · Journal of Reproductive Immunology · doi:10.1016/j.jri.2017.11.004 · Cited by 12
Pu, Y., Dong, Z., Xia, Y., et al. (2019) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2019.109382 · Cited by 12
Divergent Mast Cell Responses Modulate Antiviral Immunity During Influenza Virus Infection
Murphy-Schafer, A. R., & Paust, S. (2021) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2021.580679 · Cited by 12
Guerra, F. S., Rodrigues, D. A., Fraga, C. A. M., & Fernandes, P. D. (2021) · Pharmaceuticals · doi:10.3390/ph14050387 · Cited by 11
“IL-6 is a potent inflammatory cytokine and IL-6 can activate signal transduction through the PI3K signaling pathway [37].”
Backgroundda Conceição, A. R., Dias, K. A., Pereira, S. M. S., Saraiva, L. C., Oliveira, L. A., de Souza, E. C. G., Gonçalves, R. V., da Matta, S. L. P., Natali, A. J., Martino, H. S. D., et al. (2021) · British Journal Of Nutrition · doi:10.1017/s0007114521001355 · Cited by 12
“To date, only few studies have reported the effects of acute exercise on inflammatory pathways in the liver (2,69-71) .”
BackgroundHill, D. G., Ward, A., Nicholson, L. B., & Jones, G. W. (2021) · Cytokine · doi:10.1016/j.cyto.2021.155650 · Cited by 12
“Protein inhibitor of activated STAT (PIAS) inhibits intracellular signalling through mechanisms that include interfering with STAT proteins binding to DNA in the nucleus [12, 23].”
InfluentialExploring the Anti-Pulmonary Fibrosis Mechanism of Jingyin Granule by Network Pharmacology Strategy
Zhu, D., Yu, Q., Jiang, M., Wang, D., & Shen, Y. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.825667 · Cited by 13
Perugini, J., Mercurio, E. D., Giuliani, A., Sabbatinelli, J., Bonfigli, A. R., Tortato, E., Severi, I., Cinti, S., Olivieri, F., le Roux, C. W., et al. (2022) · Scientific Reports · doi:10.1038/s41598-022-11942-x · Cited by 17
“Multiple comparisons: (1) Obesity, Obesity and Diabetes versus Control; (2) Obesity, Obesity and Diabetes versus Control; Obesity and Diabetes versus Obesity; (3) Obesity and Diabetes versus Control, Obesity; (4) Obesity and Diabetes versus Control; (5) Obesity versus Control.”
BackgroundExploring the landscape of synthetic IL ‐6‐type cytokines
Scheller, J., Ettich, J., Wittich, C., Pudewell, S., Floss, D. M., & Rafii, P. (2023) · FEBS Journal · doi:10.1111/febs.16909 · Cited by 13
“We refer to state-of-the-art review articles for a detailed introduction to IL-6-type cytokines and their main biological functions [6,14,30].”
BackgroundResearch Progress of Interleukin-27 in Inflammatory Bowel Disease
Wang, Q., Chen, F., Peng, Y., Yi, X., He, Y., & Shi, Y. (2023) · Inflammatory Bowel Diseases · doi:10.1093/ibd/izad153 · Cited by 10
Thompson, L. H., Whiston, R., Rakhimov, Y., Taccioli, C., Liu, C., Croce, C. M., & Metcalfe, S. M. (2010) · Cell Cycle · doi:10.4161/cc.9.20.13543 · Cited by 12
Correlation of soluble gp130 serum concentrations with arterial blood pressure
Inta, I. M., Weber, D., Grundt, C., et al. (2009) · Journal of Hypertension · doi:10.1097/hjh.0b013e32831e9948 · Cited by 12
Lacreusette, A., Barbieux, I., Nguyen, J., Pandolfino, M., Dréno, B., Jacques, Y., Godard, A., & Blanchard, F. (2008) · The Journal of Pathology · doi:10.1002/path.2490 · Cited by 12
“Third, OSM and IL-6 activate the RAS/growth factor receptor-bound protein-associated binder (Gab)–phophatidylinositol 3-kinase (PI3K)/3-phosphoinositide-dependent protein kinase (PDK) 1–Akt pathway, which promotes cell proliferation and survival [19,31].”
BackgroundInfluentialCardiotrophin-1 Induces Matrix Metalloproteinase-1 in Human Aortic Endothelial Cells
Tokito, A., Jougasaki, M., Ichiki, T., & Hamasaki, S. (2013) · PLoS ONE · doi:10.1371/journal.pone.0068801 · Cited by 13
“To elucidate the signaling pathways by which CT-1 induces gene and protein expressions of MMP-1 in HAECs, we investigated the major signaling pathways for IL-6 type cytokine family, such as MAP kinase pathway and JAK/STAT cascade [31].”
BackgroundYamaji, K., Ochiai, Y., Ohnishi, K.-I., Yawata, A., Chikuma, T., & Hojo, H. (2008) · Toxicology Letters · doi:10.1016/j.toxlet.2008.04.012 · Cited by 12
Non-core Region Modulates Interleukin-11 Signaling Activity
Yanaka, S., 谷, 中., Sano, E., 野恵海子, 佐., Naruse, N., 成, 瀬., Miura, K., 浦謹一郎, 三., Futatsumori-Sugai, M., ツ森ー菅井睦美, 二., et al. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.152561 · Cited by 12
Wang, C., Qiao, W., Zhang, Y., et al. (2013) · Molecules · doi:10.3390/molecules18021775 · Cited by 12
Јovanović, J. A., Poznanović, G., Ivanović‐Matić, S., Bogojević, D., Mihailović, M., Uskoković, A. S., & Grigorov, I. (2010) · IUBMB Life · doi:10.1002/iub.313 · Cited by 12
Hong, I. K., Eun, Y., Chung, D. H., et al. (2011) · Clinical and Experimental Otorhinolaryngology · doi:10.3342/ceo.2011.4.4.193 · Cited by 12
“Once recruited, the receptor complexes allow the activation of Janus protein tyrosine kinase (JAK) and, subsequently, the activation of signal transducer and activator of transcription (STAT, mainly STAT3) and mitogen activated protein kinase (MAPK) (5-7).”
BackgroundAuernhammer, C., Dorn, F., Vlotides, G., et al. (2004) · Journal of Endocrinology · doi:10.1677/joe.0.1800479 · Cited by 12
“Receptor complexes of gp130 cytokines are constituted by ligandspecific receptor subunits and the common receptor subunit gp130 (Heinrich et al. 2003).”
BackgroundHeteroarylketones inhibit astroglial interleukin-6 expression via a STAT3/NF-κB signaling pathway
Schulz, I., Engel, C., Niestroj, A. J., Zeitschel, U., Menge, K., Kehlen, A., Meyer, A., Roßner, S., & Demuth, H. (2011) · Journal of Neuroinflammation · doi:10.1186/1742-2094-8-86 · Cited by 12
“Subsequent activation of signal tyrosine kinases of the JAK family leads to phosphorylation of pivotal signal molecules such as STAT3 and Erk1 and 2 respectively [31,32].”
BackgroundInfluentialAllergen-Induced IL-6 Regulates IL-9/IL-17A Balance in CD4+ T Cells in Allergic Airway Inflammation
Schütze, N., Trojandt, S., Kuhn, S., Tomm, J. M., von Bergen�, M., Simon, J. C., & Polte, T. (2016) · The Journal of Immunology · doi:10.4049/jimmunol.1501599 · Cited by 15
“The classical activation pathway of IL-6 receptor induces STAT3 phosphorylation (28).”
Heo, J. H., Yoon, J. A., Ahn, E. K., Kim, H., Urm, S. H., Oak, C. O., Yu, B. C., & Lee, S. J. (2017) · Journal of Tissue Engineering and Regenerative Medicine · doi:10.1002/term.2522 · Cited by 12
Role of platelet-rich fibrin on intestinal anastomosis wound healing in a rat
Özçay, N., Özdemir, B. H., & Besim, H. (2018) · Biomedical Materials · doi:10.1088/1748-605x/aab8e1 · Cited by 12
Sabry, D., Abdelaleem, O. O., Hefzy, E. M., et al. (2018) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2018.0065 · Cited by 12
Chen, Q., Shi, P., Wang, D., Liu, Q., Xu, L., Wang, Y., Zou, D., Huang, Z., Gao, X., & Lin, Z. (2019) · American Journal Of Pathology · doi:10.1016/j.ajpath.2019.01.012 · Cited by 11
Akbarian, F., Abolhasani, M., Dadkhah, F., Asadi, F., & Ahangari, G. (2019) · Current Molecular Medicine · doi:10.2174/1566524019666190709180146 · Cited by 12
Association of Variants in IL6-Related Genes with Lung Cancer Risk in Moroccan Population
Kaanane, H., Senhaji, N., Berradi, H., Benchakroun, N., Benider, A., Karkouri, M., Attar, H. E., CASA, I., Khyatti, M., & Nadifi, S. (2019) · Lung · doi:10.1007/s00408-019-00261-0 · Cited by 12
Bongartz, H., Seiß, E. A., Bock, J., & Schaper, F. (2021) · Journal of Neurochemistry · doi:10.1111/jnc.15305 · Cited by 12
“As IL- 6 signalling coordinates the immune response, dysregulated IL- 6 signalling is associated with autoimmune diseases, such as rheumatoid arthritis or multiple sclerosis (for review, see (Heinrich et al., 2003)).”
BackgroundSelf-citationCapone, A., Naro, C., Bianco, M., Bardi, M. D., Noël, F., Macchi, P., Battistini, L., Soumelis, V., Volpe, E., & Sette, C. (2021) · iScience · doi:10.1016/j.isci.2021.102492 · Cited by 12
“Thus, a comprehensive transcriptional analysis of human Th17 cells undergoing differentiation in optimal Th17 conditions (TGF-b, IL-6, IL-1b, and IL-23) (Volpe et al., 2008; Manel et al., 2008) had not been performed to date.”
BackgroundInfluentialPredictive Value of IL-6 Combined with NLR in Inflammation and Cancer
Yuan, C., Pan, Y., & Ning, Y. (2021) · Cancer Investigation · doi:10.1080/07357907.2020.1858852 · Cited by 12
“Interleukin-6 (IL-6) is one of the most highly expressed mediators of inflammation in the tumor microenvironment, which belongs to a large family of cytokines that share the common signaling gp130 receptor, whose engagement triggers activation of Janus (JAK) kinases and their downstream effectors, including STAT3, SHP…”
BackgroundZheng, J., Li, B., Yan, Y., Huang, X., & Zhang, E. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms24010444 · Cited by 13
“IL-6 is critical for hematopoiesis in the liver and good health, and dysregulated IL-6 expression can lead to diseases such as rheumatoid arthritis, osteoporosis, and cirrhosis [36].”
BackgroundMateu, A., DIOS, I. D., Manso, M. A., & Ramudo, L. (2015) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2015.09.015 · Cited by 12
Oncostatin M up-regulates the ER chaperone Grp78/BiP in liver cells
Vollmer, S., Haan, C., & Behrmann, I. (2010) · Biochemical Pharmacology · doi:10.1016/j.bcp.2010.07.015 · Cited by 12
“These Jaks (mainly Jak1) phosphorylate certain tyrosine residues within the receptor chains leading to the formation of docking sites for signaling molecules with matching SH2 domains, like signal transducers and activators of transcription (STAT) or adaptor proteins for the mitogen-activated protein kinase pathway (M…”
BackgroundInfluentialSelf-citationBonar, E., Dubin, A., BIERCZYNSKAKRZYSIK, A., et al. (2006) · Cytokine · doi:10.1016/j.cyto.2005.12.011 · Cited by 12
Malemud, C. J. (2010) · International Journal of Interferon Cytokine and Mediator Research · doi:10.2147/ijicmr.s9470 · Cited by 12
“…laudable clinical goal designed to regulate chronic inflammation, inhibition of parallel SAP/MAPK 60,62,71,72 and PI3K/Akt/mTor signaling pathways, 53 Toll-like receptor (TLR) activation, 62 and the immunoreceptor tyrosine-based activation motif pathway 73,74 may also have to be considered as a…”
InfluentialEvolutionary plasticity of IL-6 cytokine family
Gorshkova, E. A., Nedospasov, S. A., & Shilov, E. S. (2016) · Molecular Biology · doi:10.1134/s0026893316060066 · Cited by 12
Shingleton, W. D., Jones, D., Xu, X., et al. (2006) · Lara D. Veeken · doi:10.1093/rheumatology/kel024 · Cited by 12
“Oncostatin M (OSM) is a cytokine of the IL-6 family, all of which bind a common receptor, glycoprotein 130 (gp130) [13].”
BackgroundFritzenwanger, M., Foerster, M., Meusel, K., et al. (2008) · Chinese Medical Journal · doi:10.1097/00029330-200812020-00022 · Cited by 12
Yu, J., Qi, J., Kong, X., & Feng, Y. (2025) · Pharmacological Research · doi:10.1016/j.phrs.2025.107966 · Cited by 13
Rafii, P., Cruz, P. R., Ettich, J., Seibel, C., Padrini, G., Wittich, C., Lang, A., Petzsch, P., Köhrer, K., Moll, J. M., et al. (2024) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2024.107251 · Cited by 11
“2 C ) (36).”
Zhang, L., Liu, P., Jiang, Y., Fan, D., He, X., Zhang, J., Luo, B., Sui, J., Luo, Y., Fu, X.-Y., et al. (2024) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2024.116448 · Cited by 11
Manoharan, S., & Perumal, E. (2024) · Fitoterapia · doi:10.1016/j.fitote.2024.106265 · Cited by 11
Kim, S., Kim, K. H., Jung, H., Jeong, E.-O., Lee, H.-J., Kwon, J., Kwon, H., Choi, S.-W., Koh, H., & Kim, S. (2024) · Journal of Cancer · doi:10.7150/jca.104759 · Cited by 11
“Dysregulation and elevation of IL-6 have been suggested to play significant roles in the development of inflammatory and autoimmune disorders as well as cancer [29].”
MicroRNA-feedback loop as a key modulator of liver tumorigenesis and inflammation
Gougèlet, A. (2013) · World Journal of Gastroenterology · doi:10.3748/wjg.v19.i4.440 · Cited by 11
Mechanisms of JAK/STAT pathway negative regulation by the short coreceptor Eye Transformer/Latran
Fisher, K. H., Stec, W. J., Brown, S., et al. (2015) · Molecular Biology of the Cell · doi:10.1091/mbc.e15-07-0546 · Cited by 11
“Of these, the IL-6 family of vertebrate cytokine receptors, most similar to Drosophila Dome, can be broadly split into two categories: long β-receptors, such as GP130, LIFRβ, and OSMRβ, and shorter α-receptors, such as IL-6Rα, IL-11Rα, and IL-13Rα2 (Rahaman et al., 2002; reviewed in Taga and Kishimoto, 1997; Heinrich…”
InfluentialEndogenous Mechanisms of Cardiac Regeneration
Xiang, M. S. W., & Kikuchi, K. (2016) · International review of cytology · doi:10.1016/bs.ircmb.2016.04.002 · Cited by 11
STAT3 is involved in IL-6-Mediated Downregulation of Hepatic Transporters in Mice
Abualsunun, W. A., & Piquette‐Miller, M. (2018) · Journal of Pharmacy & Pharmaceutical Sciences · doi:10.18433/jpps30241 · Cited by 11
“During inflammation, secretion of IL-6 regulates the expression of numerous genes through activation of the JAK3/STAT3 signalling pathway [18].”
BackgroundIL-6 deficiency attenuates p53 protein accumulation in aged male mouse hippocampus
Bialuk, I., Cieślińska, M., Kowalczuk, O., Bonda, T. A., Nikliński, J., & Winnicka, M. M. (2019) · Biogerontology · doi:10.1007/s10522-019-09841-2 · Cited by 11
Oncostatin M Plays a Critical Role in Survival after Acute Intestinal Ischemia: Reperfusion Injury
Young, P. Y., Mueller, T., Sis, B., Churchill, T. A., & Khadaroo, R. G. (2020) · Surgical Infections · doi:10.1089/sur.2019.193 · Cited by 11
“The protein belongs to the IL-6 family of cytokines (IL-6, IL-11, IL-27, leukemia inhibitory factor [LIF], OSM, ciliary neurotrophic factor [CNTF], cardiotrophin [CT]-1, cardiotrophin-like cytokine [CLC]) that all signal through GP130 [13-17].”
High irisin and low BDNF levels in aqueous humor of high myopia
Wang, X., Li, M., Zheng, R., Cui, T., Qin, J., Su, Z., Shang, M., & Bao, Y. (2021) · Advances in Clinical and Experimental Medicine · doi:10.17219/acem/125428 · Cited by 11
Interleukin 6/gp130 axis promotes neural invasion in pancreatic cancer
Suzuki, H., Mitsunaga, S., Ikeda, M., Aoyama, T., Yoshizawa, K., Yamaguchi, M., Suzuki, M., Narita, M., Kawasaki, T., & Ochiai, A. (2022) · Cancer Medicine · doi:10.1002/cam4.4823 · Cited by 10
Rafii, P., Seibel, C., Weitz, H. T., Ettich, J., Minafra, A. R., Petzsch, P., Lang, A., Floss, D. M., Behnke, K., Köhrer, K., et al. (2023) · Communications Biology · doi:10.1038/s42003-023-04768-4 · Cited by 10
Zhao, H., Yan, W. H., Miaona, J., Zhang, C., Shen, L., & Jia, Y. (2009) · Pathology - Research and Practice · doi:10.1016/j.prp.2009.02.010 · Cited by 11
Oncostatin M as a target biological molecule of preeclampsia
Lee, G., Kil, G. C., Kwon, J., et al. (2009) · Journal of obstetrics and gynaecology research · doi:10.1111/j.1447-0756.2009.01114.x · Cited by 11
“OSM is a member of the IL-6 family which comprise IL-6, IL-11, OSM, ciliary neutrophic factor, and leukemia-inhibitory factor (LIF).(12) OSM has many unique biological activities in inflammation, hematopoiesis, development and inhibiting the proliferation of tumor cells.”
BackgroundKondaurova, E. M., Naumenko, V. S., Sinyakova, N. A., & Kulikov, A. V. (2010) · Journal of Neuroscience Research · doi:10.1002/jnr.22545 · Cited by 11
“The Il6st gene encodes the gp130 protein, which is the signal transducer subunit in receptors of the gp130-related cytokines such as IL-6, IL-11, and IL-27, ciliary neurotrophic factor, cardiotrophin-like cytokine, and neurotrophin (Chesnokova and Melmed, 2002; Heinrich et al., 2003; Fasnacht and Muller, 2008).”
BackgroundFitzGerald, L., Macey, P. M., & Brecht, M. (2012) · PLoS ONE · doi:10.1371/journal.pone.0040513 · Cited by 12
TLR3 ligation protects human astrocytes against oxidative stress
Borysiewicz, E., Doppalapudi, S., Kirschman, L. T., & Konat, G. W. (2012) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2012.11.002 · Cited by 11
“STAT3 is an important intracellular signal protein downstream from the interleukin 6 signal transducer (IL6ST), a common subunit of receptor complexes for the IL-6 superfamily of cytokines (Hirano et al., 2000; Heinrich et al., 2003).”
gp130 Activation in Müller Cells is Not Essential for Photoreceptor Protection from Light Damage
Ueki, Y., Chollangi, S., Le, Y.-Z., & Ash, J. D. (2009) · Advances in experimental medicine and biology · doi:10.1007/978-1-4419-1399-9_75 · Cited by 11
“Activated gp130 signals through the Jak/STAT3, ERK1/2, and PI3K/Akt pathways (Boulton et al. 1994; Heinrich et al. 2003; Oh et al. 1998).”
BackgroundCardiotrophin‐1 decreases intestinal sugar uptake in mice and in C aco‐2 cells
Lópeź‐Yoldi, M., Castilla‐Madrigal, R., Lostao, M. P., et al. (2016) · Acta Physiologica · doi:10.1111/apha.12674 · Cited by 11
“The activation of the gp130 receptor leads to phosphorylation of STAT3, the signalling effector of rCT-1 (Heinrich et al. 2003).”
BackgroundCurrent Status of Thalidomide and CC-5013 in the Treatment of Metastatic Prostate Cancer
Sissung, T. M., Þórðardóttir, S., Gardner, E. R., & Figg, W. D. (2009) · Anti-Cancer Agents in Medicinal Chemistry · doi:10.2174/187152009789735017 · Cited by 11
Al‐Quraishy, S., Dkhil, M. A., Abdel‐Baki, A. S., et al. (2017) · Parasitology Research · doi:10.1007/s00436-017-5423-0 · Cited by 11
“For, GP130 is known to act as the common signal transducer for the polyfunctional interleukin 6 class cytokine family, consisting of IL-6, IL-11, cardiotrophin1 (CT-1), oncostatin M (OSM), ciliary neurotrophic factor (CNTF), cardiotrophin-like cytokine (CLC), and leukemia inhibitory factor (LIF) (Heinrich et al. 2003).”
BackgroundMayati, A., Moreau, A., Denizot, C., Stieger, B., Parmentier, Y., & Fardel, O. (2017) · European Journal of Pharmaceutical Sciences · doi:10.1016/j.ejps.2017.06.010 · Cited by 12
Functional repertoire of interleukin-6 in the central nervous system – a review
Heese, K. (2017) · Restorative Neurology and Neuroscience · doi:10.3233/rnn-170772 · Cited by 11
“The IL-6 receptor family comprises multi-subunit receptors, including the ciliary neurotrophic factor receptor (CNTFR) and leukemia inhibitory factor receptor (LIFR), associated with a common receptor subunit, the transmembrane protein gp130 (Heinrich et al., 2003; Taga & Kishimoto, 1997).”
Johnston, P. A., Sen, M., Hua, Y., Camarco, D. P., Shun, T. Y., Lazo, J. S., & Grandis, J. R. (2017) · Methods in molecular biology · doi:10.1007/978-1-4939-7357-6_14 · Cited by 11
Metadata
- Authors
- HEINRICH, P. C., BEHRMANN, I., HAAN, S., HERMANNS, H. M., MÜLLER-NEWEN, G., & SCHAPER, F.
- Affiliations
- Universitätsklinikum Aachen (DE)
- Institut für Biochemie, RWTH Aachen, Universitätsklinikum, Pauwelsstrasse 30, D-52074 Aachen, Germany
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2003-08-15
- Volume
- 374
- Issue
- 1
- Pages
- 1-20
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC1223585
- OpenAlex
- W2086840459
- Cited by
- 3,272
- References
- 265
- Citations by year
- 2026: 70 · 2025: 114 · 2024: 106 · 2023: 121 · 2022: 138 · 2021: 146 · 2020: 129 · 2019: 151 · 2018: 141 · 2017: 141 · 2016: 176 · 2015: 157 · 2014: 171 · 2013: 190 · 2012: 179
- FWCI
- 50.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biochemical Journal (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- cytokine signaling, gp130, LIF receptor, OSM receptor, JAK/STAT signaling, MAPK signaling, protein tyrosine phosphatase, suppressor of cytokine signaling, PIAS, signal termination, signal transduction, acute phase response, inflammation, rheumatoid arthritis, multiple myeloma, prostate cancer
- MeSH terms
- Animals, Humans, Infections, Models, Molecular, Phosphorylation, Protein Conformation, Wounds and Injuries, Signal Transduction, Interleukin-6, Cytokines, Protein Structure, Secondary, Receptors, Interleukin-6
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