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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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A new protein containing an SH2 domain that inhibits JAK kinases
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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
Chung, C. D., Liao, J., Liu, B., Rao, X., Jay, P., Berta, P., & Shuai, K. (1997) · Science · doi:10.1126/science.278.5344.1803 · Cited by 980
Cited by
Sorted by citations
Items 2,401–2,500 of 3,269
Smith, S. C., & Ascione, R. (2023) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2023.108397 · Cited by 5
“However,whereasIL-6/gp130signallingoccursviathecanonical Jak-STAT pathway, the IL-11 receptor complex predominantly activates the non-canonical pathway via ERK in mouse and human cardiac fi bro-blasts (Heinrich et al., 2003; Schafer et al., 2017).”
BackgroundRefaie, M. M. M., Rifaai, R. A., Bayoumi, A. M. A., et al. (2023) · Journal of Pharmacy and Pharmacology · doi:10.1093/jpp/rgad049 · Cited by 5
Peiris, R. M., May, C. N., Booth, L. C., McAllen, R. M., McKinley, M. J., Hood, S. G., Martelli, D., Bellomo, R., & Lankadeva, Y. R. (2023) · Intensive Care Medicine Experimental · doi:10.1186/s40635-023-00530-6 · Cited by 5
“Monocytes, macrophages, and neutrophils contain IL-6 receptors, and their function is regulated by IL-6 signaling pathways [32].”
BackgroundGirdhar, A., Raju, K., & Prasad, K. K. (2023) · Biomedical Research and Therapy · doi:10.15419/bmrat.v10i8.826 · Cited by 5
Shin, S. K., Hong, E.-J., Lee, J.-H., Kim, K.-Y., Choi, J.-Y., & Kim, K. M. (2023) · Journal of the Korean Society of Food Science and Nutrition · doi:10.3746/jkfn.2023.52.11.1101 · Cited by 5
Dienogest attenuates STAT3 activation in ovarian endometriotic cysts
Choi, J., Jo, M., Lee, E., Kim, S. E., Lee, D., & Choi, D. (2024) · European Journal of Obstetrics & Gynecology and Reproductive Biology · doi:10.1016/j.ejogrb.2024.01.013 · Cited by 5
Köning, T., & Calaf, G. M. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25168604 · Cited by 5
“The Interleukin 6 (IL6)-like family is a group of proteins with similar structure and functional features, and IL6 signal transducer (IL6ST, which is also its gene name) is a transmembrane signaling receptor that acts as a signal transducer in all signaling by this cytokine family [30,31].”
BackgroundPost-Acute Sequelae and Mitochondrial Aberration in SARS-CoV-2 Infection
Ward, C., & Schlichtholz, B. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25169050 · Cited by 5
“…the anti-inflammatory effects of IL-6, a cytokine that, via the JAK/STAT pathway, activates genes involved in differentiation, survival, apoptosis and proliferation [131] and viral targeting of parts of the JAK/STAT pathway results in both interferon dysfunction and insensitivity to IL-6 [132].”
BackgroundAlserhani, G. S., Mohamed, M. E., & Younis, N. S. (2025) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-025-04042-w · Cited by 5
“JAK/STAT signaling pathway synchronizes numerous biological actions such as cell proliferation, differentiation, inflammation, and apoptosis (Heinrich et al. 2003).”
Role of Cytokines and Chemokines in HIV Infection
Venketaraman, V., Morris, D., Donohou, C., et al. (2011) · InTech eBooks · doi:10.5772/20322 · Cited by 5
Regulation of JAKs: Insights Gleaned from the Functional Protein Domains
Haan, C., Ungureanu, D., Pekkala, T., et al. (2012) · Springer eBooks · doi:10.1007/978-3-7091-0891-8_2 · Cited by 5
“Cytokine receptors bind different JAKs (Heinrich et al. 2003; O’Sullivan et al. 2007; Pestka et al. 2004; Kovanen and Leonard 2004; Hintzen et al. 2008) and the specificity”
BackgroundSelf-citationGangavarapu, K. J., Olbertz, J., Bhushan, A., et al. (2008) · APOPTOSIS · doi:10.1007/s10495-008-0265-y · Cited by 5
DiScipio, R. G., Khaldoyanidi, S. K., & Schraufstätter, I. U. (2011) · Protein Expression and Purification · doi:10.1016/j.pep.2011.04.016 · Cited by 5
“LIF is known to cause activation of the LIF receptor/GP130 complex, which results in the phosphorylation of STAT-3 [57,58].”
BackgroundMirowska-Guzel, D. M., Gromadzka, G., Kurowska, K., et al. (2010) · Immunopharmacology and Immunotoxicology · doi:10.3109/08923970903486625 · Cited by 5
“The modulation of pleiotropic cytokines such as IL-6 and IL-8 may be central to GS effect, because these molecules exert a wide range of proinflammatory as well as neurotoxic and neuroprotective effects.((7,8)) Clinical studies have detected a significant upregulation of IL-6 within active MS lesions((9,10)) as well a…”
BackgroundMühl, B., Hägele, J., Tasdogan, A., Loula, P., Schuh, K., & Bundschu, K. (2015) · Developmental Dynamics · doi:10.1002/dvdy.24261 · Cited by 5
“complex activates at least three pathways, including JAK/STAT (Janus kinase/signal transducer and activator of transcription), PI3K (phosphatidylinositol-3-phosphate kinase), and ERK/MAPK (extracellular signal-regulated kinase/mitogen-activated protein kinase) pathways (Akira et al., 1994; Boeuf et al., 1997; Niwa et…”
BackgroundElhannan, S. E., Taha, S., Khalaf, N. B., et al. (2015) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2015.2376 · Cited by 5
“The signaling pathways known to be involved in the production of IL-6 have been mainly found to be the MAPK and/or JAK/STAT pathways (18).”
Huang, C.-Y., Chen, W., Tsay, Y., Hsieh, S., Lin, Y., Lee, W., Sheu, W. H., & Chiang, A.-N. (2015) · Journal of Biomedical Science · doi:10.1186/s12929-015-0118-2 · Cited by 5
“STAT3 is an acute-phase response factor activated by phosphorylation at Tyr705, such activation leads to IL-6 regulation of many acutephase protein genes [51].”
BackgroundKumar, H., Tichkule, S., Raj, U., Gupta, S. K., Srivastava, S., & Varadwaj, P. K. (2016) · 3 Biotech · doi:10.1007/s13205-015-0357-7 · Cited by 5
“Formation of this complex results in the dime formation of the complex IL6- gp80- gp130- JAK to form (IL6- gp80gp130- JAK)2 (Heinrich et al. 2003).”
BackgroundHe, X., Pan, W., Yao, Y., et al. (2016) · Chinese Journal of Integrative Medicine · doi:10.1007/s11655-016-2526-x · Cited by 5
Yoshimatsu, G., Shahbazov, R., Saracino, G., Lawrence, M. C., Kim, P. T., Onaca, N. N., Beecherl, E. E., Naziruddin, B., & Levy, M. F. (2017) · The American Journal of Surgery · doi:10.1016/j.amjsurg.2017.03.007 · Cited by 5
Zhan, K., Jiang, M., Sui, Y., et al. (2017) · In Vitro Cellular & Developmental Biology - Animal · doi:10.1007/s11626-017-0143-4 · Cited by 5
Rheopheresis as a causal therapy option for systemic scleroderma (SSc)
Lutze, S., Daeschlein, G., Konschake, W., et al. (2017) · Clinical Hemorheology and Microcirculation · doi:10.3233/ch-179204 · Cited by 5
Wound fluid enhances cancer cell proliferation via activation of STAT3 signal pathway in vitro
Scherzad, A., Gehrke, T. E., Meyer, T. J., Ickrath, P., Bregenzer, M., Eiter, R., Hagen, R., Kleinsasser, N. H., & Hackenberg, S. (2019) · Oncology Reports · doi:10.3892/or.2019.7047 · Cited by 5
Differentiation of Tumorigenic C6 Glioma Cells Induced by Enhanced IL-6 Signaling
Chu, I.-R., Pan, R.-L., & Yang, C. S. (2020) · Medicina · doi:10.3390/medicina56110625 · Cited by 4
“The IL-6 receptor (IL-6R) is composed of two subunits, IL-6Rα and glycoprotein 130 (gp130) [25].”
BackgroundInfluentialGijsen, H. S. (2021) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-55035-6_16 · Cited by 6
Elfawy, D. M., Elkalek, M. A., Hamed, E., et al. (2021) · Ain-Shams Journal of Anaesthesiology · doi:10.1186/s42077-021-00141-x · Cited by 5
“…1ICU and Pain Management, Faculty of Medicine, Ain Shams University, Cairo, Egypt Full list of author information is available at the end of the article of IL-6 among other ARDS biomarkers is shown to have a significant impact in relation to the course of ARDS (Peter et al. 2003).”
BackgroundSamanta, S. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-821232-5.00011-2 · Cited by 5
Jin, X. C., Huang, Y., Yoo, H., Lee, S. Y., Chun, Y. S., Hong, K. Y., & Chang, H. (2022) · Aesthetic Plastic Surgery · doi:10.1007/s00266-022-03021-3 · Cited by 5
Comparison of the efficacy of gossypol acetate enantiomers in rats with uterine leiomyoma
Yuan, J., Zhou, M., Xin, X., et al. (2022) · Journal of Natural Medicines · doi:10.1007/s11418-022-01644-z · Cited by 5
“Due to the generation of UL, a large number of inflammatory mediators will be produced in uterus tissues, and cause the decline of immune regulation function of the body [44, 45].”
BackgroundThe Role of Interleukin-6/GP130 Cytokines in Cancer Cachexia
Jengelley, D. H. A., & Zimmers, T. A. (2022) · Springer eBooks · doi:10.1007/978-3-031-09518-4_6 · Cited by 6
da Costa, A. G., Franco-Duarte, R., Machado, R., & Gomes, A. (2022) · Protein Science · doi:10.1002/pro.4469 · Cited by 3
“That is the case for proteins that bind to LIFR.”
BackgroundInfluentialOkafor, C. G., Okafor, C. G., Eleje, G. U., et al. (2023) · SAGE Open Medicine · doi:10.1177/20503121231158220 · Cited by 5
Lester, L. B. (2005) · Humana Press eBooks · doi:10.1385/1592599001 · Cited by 5
Wang, G.-H., Zou, G.-X., Xian-min, Y., et al. (2017) · Biomedical Research-tokyo · Cited by 5
Chernukha, I. M., Fedulova, L., Vasilevskaya, E. R., et al. (2017) · Potravinarstvo Slovak Journal of Food Sciences · doi:10.5219/590 · Cited by 5
“…set of bands correspond interleukins: IL-2 (15.2 kDa), interleukin 15 (18.4 kDa), interleukin 6 (21.1 kDa), interleukin 23 subgroups 19 (21.13 kDa), which are directly involved in the immune response (Liao, Lin and Leonard, 2011; DePaolo et al., 2011; Heinrich et al., 2003; Yen et al., 2006).”
BackgroundInfluentialAl‐Quraishy, S., Dkhil, M. A., Abdel‐Baki, A. S., Delić, D., & Wunderlich, F. T. (2018) · Parasitology Research · doi:10.1007/s00436-018-5789-7 · Cited by 5
Zeković, A., Vreća, M., Spasovski, V., Andjelković, M., Pavlović, S., & DAMJANOV, N. S. (2018) · Clinical Rheumatology · doi:10.1007/s10067-018-4163-6 · Cited by 5
Transcriptome-based analysis of putative allergens of Chorioptes texanus
He, R., Gu, X., Xie, Y., Peng, X., Angel, C., & Yang, G. (2019) · Parasites & Vectors · doi:10.1186/s13071-019-3843-7 · Cited by 5
Corrêa, L. B., Henriques, M. D. G., Rosas, E. C., & Santos‐Oliveira, R. (2021) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-021-05515-9 · Cited by 5
“Among the cytokines, interleukin-6 (IL-6) has great effect in synovitis, with impact on bone erosions, and the whole inflammation progress [52–54], since the dysregulated continual synthesis contribute to chronic inflammation and autoimmunity [55, 56].”
BackgroundSäftig, P., & Hartmann, D. (2006) · Springer eBooks · doi:10.1007/0-387-25151-0_5 · Cited by 5
Gene engineering biological therapy for juvenile arthritis
Михельс, Х., Никишина, И. П., Федоров, Е. С., Salugina, S. O., Michels, H., Никишина, И. П., Федоров, Е. С., & Salugina, S. O. (2011) · Rheumatology Science and Practice · doi:10.14412/1995-4484-2011-873 · Cited by 5
Preformed STAT3 transducer complexes in human HepG2 cells and rat hepatocytes
Dráber, P., Dráber, P., Dráberová, L., et al. (2007) · Cellular Signalling · doi:10.1016/j.cellsig.2007.07.018 · Cited by 5
Characterization of Proteasome Inhibition on Astrocytes Cell Cycle
Ren, Q., Yu, Y., Luo, X., et al. (2008) · Journal of Molecular Neuroscience · doi:10.1007/s12031-008-9161-8 · Cited by 5
“IL-6 can bind to the signal transducer gp130 (Heinrich et al. 2003).”
BackgroundLiu, J., Briggs, M. R., & Kraemer, F. B. (2006) · Future Cardiology · doi:10.2217/14796678.2.5.605 · Cited by 5
Angelucci, F., Batocchi, A. P., Caggiula, M., et al. (2006) · NeuroImmunoModulation · doi:10.1159/000095762 · Cited by 5
“in this study we wanted to investigate in vivo the effect of short- and long-term treatment with mitoxantrone on the spontaneous production of proinflammatory cytokines [interleukin (IL)-6 and IL-12p40] and anti-inflammatory cytokines [IL-10 and transforming growth factor-β(TGF-β)] in a population of secondary progres…”
BackgroundImpact of STAT/SOCS mRNA Expression Levels after Major Injury
Brumann, M., Matz, M., Kusmenkov, T., Stegmaier, J., Biberthaler, P., Kanz, K., Mutschler, W., & Bogner, V. (2014) · Mediators of Inflammation · doi:10.1155/2014/749175 · Cited by 5
SOCS3 Modulates Interleukin-6R Signaling Preference in Dermal Fibroblasts
Luckett‐Chastain, L. R., Ihnat, M. A., Mickle, B. M., & Gallucci, R. M. (2012) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2011.0086 · Cited by 5
Negative modulation of signal transduction via interleukin splice variation
Denessiouk, K. A., Denesyuk, A. I., & Johnson, M. S. (2007) · Proteins Structure Function and Bioinformatics · doi:10.1002/prot.21756 · Cited by 5
Inhibition of pro-inflammatory cytokine receptor signalling by cAMP in vascular endothelial cells
Sands, W. A., & Palmer, T. M. (2005) · Biochemical Society Transactions · doi:10.1042/bst0331126 · Cited by 6
Clerk, A., Cullingford, T. E., Fuller, S. J., et al. (2009) · Advances in Enzyme Regulation · doi:10.1016/j.advenzreg.2008.12.007 · Cited by 5
“A. Clerk 15 IL6 family cytokines (which includes cardiotrophin-1 and Lif) stimulate gp130 receptors (Müller-Newen, 2003) to activate JAK/STAT signalling and signalling through the ERK5 cascade (Heinrich et al., 2003).”
BackgroundGong, K., ZHANG, H., Du, J., & Zhang, Y. (2007) · Acta Pharmacologica Sinica · doi:10.1111/j.1745-7254.2007.00525.x · Cited by 5
Cholera toxin B induced activation of murine macrophages exposed to a fixed bacterial immunogen
Wiedinger, K., Romlein, H., & Bitsaktsis, C. (2015) · Therapeutic Advances in Vaccines · doi:10.1177/2051013615613473 · Cited by 5
“IL-6 is a proinflammatory cytokine which enhances the innate immune system through the induction of acute phase proteins and stimulation of T and B lymphocytes [Heinrich et al. 2003].”
BackgroundNew insights into airway mucous cell differentiation
Wu, R., Harper, R. W., Kao, C., Thai, P., Wu, D., Chen, Y., & Chang, M. M. (2006) · Journal of Organ Dysfunction · doi:10.1080/17471060600580672 · Cited by 5
Zhu, Z., Turak, A., Xu, N., Jenis, J., & Aisa, H. A. (2024) · Fitoterapia · doi:10.1016/j.fitote.2024.106335 · Cited by 5
Qu, Q., Liu, S.-Y., Fu, B., Ao, Q., Long, Y., Liu, Z., Wei, W., Hou, W., Liu, X., & Tian, X. (2025) · Stem Cell Research & Therapy · doi:10.1186/s13287-025-04744-1 · Cited by 6
“Given the critical role of IL-6 signaling in Th17 differentiation via the IL-6R/JAK1/STAT3 axis [55–57], we further investigated this pathway.”
Du, L., Cheng, X., Liu, B., Hao, Y., Long, Z., Hu, Q., Huo, B., Xie, T., Cheng, Q., Zhou, Y., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262412061 · Cited by 5
“…patients) alone could upregulate the expression of multiple cytokine genes; moreover, the mRNA levels of inflammatory cytokines (IL-1 β [69], IL-6 [70], TNF-α [71]), epithelial cytokines (IL-25 [72]) and type 2 immune response-related cytokines (IL-5) in mice co-treated with both microorganisms…”
Interleukin-6: A Central Biomarker in Adult and Pediatric Cancer and Infectious Disease
Benedetto, G. D., Sorice, C., Cantiello, I., Savarese, M., Leone, O., Capozza, M. A., & Alfieri, M. (2026) · Biologics · doi:10.3390/biologics6010005 · Cited by 5
“…tissue repair, and regeneration, chronic or dysregulated IL-6 signaling promotes persistent inflammation, autoimmunity, fibrosis, and tissue damage, contributing to the pathogenesis of disorders such as rheumatoid arthritis, inflammatory bowel disease, and cytokine-driven malignancies [12,13].”
Liu, H., Li, Q., Li, J., et al. (2026) · Frontiers in Oncology · doi:10.3389/fonc.2026.1761266 · Cited by 4
Klos, B., Patel, P., Rose, C. E., Bush, T. J., Conley, L. J., Kojic, E., Henry, K., Brooks, J., Hammer, J., & the SUN study investigators (2019) · HIV Medicine · doi:10.1111/hiv.12754 · Cited by 3
Defining a novel DYRK1A-gp130/IL-6R-pSTAT axis that regulates Th17 differentiation
Malueg, M., Moo, K. G., Arnett, A., Edwards, T. H., Ruskin, S. L., Lambert, K., Subramanyam, A., Dufort, M. J., Gersuk, V. H., Partridge, R., et al. (2025) · ImmunoHorizons · doi:10.1093/immhor/vlae005 · Cited by 6
Yang, Y. J., Kim, M. J., Heo, J. W., Choi, H. N., Lee, D., Kim, Y., & Park, K. (2025) · Molecular & Cellular Toxicology · doi:10.1007/s13273-025-00531-4 · Cited by 5
“IL-6 is a soluble mediator that exerts pleiotropic effects on inflammation and immune response, and is frequently detected in chronic inflammatory diseases (Heinrich et al. 2003; Tanaka et al. 2014).”
Long, K., Xiang, K., Zeng, Q., & Dong, W. (2025) · European Journal of Histochemistry · doi:10.4081/ejh.2025.4176 · Cited by 4
“…that the mechanism by which SOCS regulates JAK/STAT to inhibit tumor progression is also dysregulated with cytokine receptors, Toll-like receptors, and hormone receptors signaling, 39-41 IL-6, 42 long non-coding RNAs, 43 TME, 42,44 insulin-like growth factor-I, 45 and immune checkpoint molecules.”
InfluentialMing, S., Ou, J., Huang, Y., Tang, Z., Qin, Y., Ma, H., Gan, S., & Li, Z. (2025) · Open Life Sciences · doi:10.1515/biol-2025-1106 · Cited by 4
“By measuring the levels of IL-1 β , IL-6, and TNF-α , one can comprehensively assess the severity of in fl ammation in the body [25,27].”
Kalpachidou, T., Kummer, K. K., Handle, V., Zimmermann, D., Peteinareli, M., Quarta, S., Schiefermeier-Mach, N., Castaldi, L., Heppenstall, P. A., Haberberger, R. V., et al. (2025) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2025.102670 · Cited by 4
“23 17, these Recently, a particular group of microRNAs (miRNAs), including miR-21, miR-431, and miR-511, all of which are controlled by IL-6 in sensory neurons, offer new potential for IL-6-mediated mechanistic insights.”
Pudewell, S., Heuser, J., Dorogobed, I., Lipinski, B., Tran, T. H. H., Metzenmacher, P., Kunze, R., Geyer, F. K., Zielonka, S., Floss, D. M., et al. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1613004 · Cited by 5
Vullo, C., Crupi, R., Paola, R. D., et al. (2022) · Veterinary Sciences · doi:10.3390/vetsci9120664 · Cited by 4
“IL‐6 exhibits a pleiotropic effect which involves an important activation of the immune system response [16], studies demonstrate that elevated IL‐6 levels in the postoperative periods are associated with a negative outcome of surgery and with an in‐ creased systemic inflammatory response [17].”
BackgroundShi, X., Yu, J., Lü, Q., et al. (2023) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.17878 · Cited by 4
Cytokines in normal pregnancy and miscarriage
Zamyatina, S. V., Elchaninova, S. A., Михайловна, Р. В., Dudareva, Y. A., & Викторовна, Р. Т. (2024) · Russian Journal of Human Reproduction · doi:10.17116/repro20243001172 · Cited by 5
Cao, M., & Cui, B. (2024) · Cardiovascular Diabetology · doi:10.1186/s12933-024-02222-1 · Cited by 5
Zhang, H. (2024) · Mediterranean Journal of Hematology and Infectious Diseases · doi:10.4084/mjhid.2024.052 · Cited by 4
“34,35 In this study, it was observed that patients with CAL exhibited significantly elevated levels of IL-6, which aligns with findings from previous studies conducted by other researchers.”
ResultWang, B.-F., Wang, Y.-Y., Lin, H. P., & Yi, Y.-L. (2024) · Tissue Barriers · doi:10.1080/21688370.2024.2399235 · Cited by 4
“16,32 Previous studies have indicated that the STAT3 pathway plays a crucial role in host defense responses and the maintenance of barrier function.”
Lu, J., Yin, Z., Qiu, Y., Yang, Y., Chen, Z., Wu, J., & Wang, Z. (2025) · Biomedicines · doi:10.3390/biomedicines13040957 · Cited by 4
“Therefore, our study did not require a separate ethical review and approval.”
Fu, X., Ren, L., Chen, J., Liao, K., Fu, Y., Qian, X., & Xiao, J. (2015) · Asia-Pacific Journal of Clinical Oncology · doi:10.1111/ajco.12357 · Cited by 5
Fakhoury, I., & Gali‐Muhtasib, H. U. (2011) · InTech eBooks · doi:10.5772/24404 · Cited by 4
“IL-6 secreted by the macrophages releases proteinases and elastases which bind to IL-6 receptor and generate signals implicated in humoral inflammation (Heinrich et al., 2003).”
BackgroundRefining the Management of Rheumatoid Arthritis: the Benefits of Subcutaneous Tocilizumab
Negoescu, A., & Östör, A. (2014) · Rheumatology and Therapy · doi:10.1007/s40744-014-0007-2 · Cited by 3
“and T and B cells [8, 24–26].”
Osuka, K., Watanabe, Y., Aoyama, M., et al. (2014) · Journal of Neuroinflammation · doi:10.1186/s12974-014-0142-2 · Cited by 4
“of immediate early genes [5].”
STAT3 Nuclear Egress Requires Exportin 7 via Engaging Lysine Acetylation
Yu, A. H. H. (2014) · MOJ Cell Science & Report · doi:10.15406/mojcsr.2014.01.00004 · Cited by 4
Menezes, G. D., Goulart, V. G., Espírito‐Santo, S., Oliveira-Silva, P., Serfaty, C. A., & Campello‐Costa, P. (2016) · NeuroImmunoModulation · doi:10.1159/000444529 · Cited by 4
Branislav, S. (2013) · Journal of Clinical & Experimental Cardiology · doi:10.4172/2155-9880.s7-003 · Cited by 4
“ISSN:2155-9880 JCEC, an open access journal Advances in Cardiac Surgery and Therapeutics J Clin Exp Cardiolog Low concentrations of IL-6 indicates a complete absence of immune activation in first-operated [28], whereas in re-operated there was some degree of immunoreactivity (p = 0.”
BackgroundBernard, J. J. (2014) · Journal of Carcinogenesis & Mutagenesis · doi:10.4172/2157-2518.1000183 · Cited by 4
“MCP-1, leptin, ICAM-1, and IL-6 have all been shown to inhibit apoptosis and stimulate proliferation in a wide range of cell types [32-34] and levels are elevated in obesity and in some cancers [35-38].”
BackgroundSritharan, S., Kannan, T., Mn, N., & Nurul, A. A. (2014) · IIUM Medical Journal Malaysia · doi:10.31436/imjm.v13i2.474 · Cited by 4
Zhang, Z., Chen, Y.-J., Xiang, L., Pan, J., Wang, Z., Xiao, G. G., & Ju, D. (2017) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2017.3130 · Cited by 4
“Another signaling cascade activated by cytokines of the IL-6 family is the phosphoinositide-3-kinase/AKT (27,28).”
BackgroundBlanco-Favela, F. A., Espinosa-Luna, J. E., Chávez-Rueda, A. K., Madrid-Miller, A., & Chávez-Sanchéz, L. (2017) · Archives of Medical Research · doi:10.1016/j.arcmed.2017.11.001 · Cited by 4
Control of Liver Gene Expression by Sex Steroids and Growth Hormone Interplay
Fernández‐Pérez, L., de Mirecki-Garrido, M., Recio, C., & Guerra, B. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.86611 · Cited by 4
Banerjee, A., Dasgupta, R., & Ray, S. (2019) · International Journal of Peptide Research and Therapeutics · doi:10.1007/s10989-019-09996-z · Cited by 4
Oshitari, T. (2021) · Expert Review of Ophthalmology · doi:10.1080/17469899.2021.1912595 · Cited by 4
“IL-6 binds to gp130 homodimers which are expressed in RGCs of the adult retina [38].”
BackgroundInfluentialZhou, B., Li, S., Ye, J., Liu, Y., Hu, L., Tang, Y., Wu, Z., & Zhang, P. (2021) · International Immunopharmacology · doi:10.1016/j.intimp.2021.108254 · Cited by 4
Zar, A., Ahmadi, F., Karimi, F., Ahmadi, M., & Ramsbottom, R. (2022) · Molecular & cellular biomechanics · doi:10.32604/mcb.2022.018345 · Cited by 4
Donath, S., Angerstein, L., Gentemann, L., Müller, D., Seidler, A., Jesinghaus, C., Bleich, A., Heisterkamp, A., Büettner, M., & Kalies, S. (2022) · Cells · doi:10.3390/cells11071143 · Cited by 4
“Il6 is involved in immediate answer to injury and infection [58].”
BackgroundRay, S., & Luharuka, S. (2022) · Protein and Peptide Letters · doi:10.2174/0929866529666220405102230 · Cited by 4
Tatsuda, D., Yoshida, J., Ohishi, T., et al. (2023) · Anticancer Research · doi:10.21873/anticanres.16415 · Cited by 4
Mukherjee, S., Ghosh, S., Bawali, S., Chatterjee, R., Saha, A., Sengupta, A., Keswani, T., Sarkar, S., Ghosh, P., Chakraborty, S., et al. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.110671 · Cited by 4
Amato, B., Ippolito, D., Vitale, M., et al. (2024) · Microorganisms · doi:10.3390/microorganisms12020407 · Cited by 4
Immunology and targeted therapy in Castleman disease
Tsunoda, S., Harada, T., Kikushige, Y., Kishimoto, T., & Yoshizaki, K. (2024) · Expert Review of Clinical Immunology · doi:10.1080/1744666x.2024.2357689 · Cited by 4
Oliboni, L., Casarin, J. N., & Chielle, E. O. (2016) · Clinical & Biomedical Research · doi:10.4322/2357-9730.65335 · Cited by 5
Jalvy, S., Veschambre, P., Fédou, S., Rezvani, H. R., Thézé, N., & Thiébaud, P. (2018) · Developmental Biology · doi:10.1016/j.ydbio.2018.12.020 · Cited by 4
Interleukin-6 Receptor Asp358 A>C Polymorphism Is Associated With Postoperative Atrial Fibrillation
Wu, F., Feng, X., Wu, Y., Yu, M., Ding, S., & Zhao, H. (2020) · The Annals of Thoracic Surgery · doi:10.1016/j.athoracsur.2020.04.123 · Cited by 4
Adipokines in dental pulp: Physiological, pathological, and potential therapeutic roles
Álvarez-Vásquez, J. L., Guapisaca, M. I. B., Gavidia-Pazmiño, J. F., & Morales, R. V. I. (2021) · Journal of Oral Biosciences · doi:10.1016/j.job.2021.11.002 · Cited by 4
Jak/STAT Signaling in Head and Neck Cancer
Cedars, E., Johnson, D. E., & Grandis, J. R. (2018) · Current cancer research · doi:10.1007/978-3-319-78762-6_6 · Cited by 4
Effect of Poly(methacrylic acid) on the Cytokine Level in an In Vivo Tumor Model
Zhukova, O., Arkhipova, E., Kovaleva, T., Zykova, D., & Dubovskaya, N. A. (2022) · Molecules · doi:10.3390/molecules27144572 · Cited by 4
“IL-6 plays a substantial role in the pathogenesis of cancer and is known to induce the synthesis and secretion of acute-phase proteins [11].”
Background
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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