The DOI matches its Crossref record; 55 of the 59 references it cites were found in a registry or an index; none of the 40 sources its claims cite is checked for support yet.
The transcription factor PU.1 is involved in macrophage proliferation.
Open accessAbstract
PU.1 is a tissue-specific transcription factor that is expressed in cells of the hematopoietic lineage including macrophages, granulocytes, and B lymphocytes. Bone marrow-derived macrophages transfected with an antisense PU.1 expression construct or treated with antisense oligonucleotides showed a decrease in proliferation compared with controls. In contrast, bone marrow macrophages transfected with a sense PU.1 expression construct displayed enhanced macrophage colony-stimulating factor (M-CSF)-dependent proliferation. Interestingly, there was no effect of sense or antisense constructs of PU.1 on the proliferation of the M-CSF-independent cell line, suggesting that the response was M-CSF dependent. This was further supported by the finding that macrophages transfected with a sense or an antisense PU.1 construct showed, respectively, an increased or a reduced level of surface expression of receptors for M-CSF. The enhancement of proliferation seems to be selective for PU.1, since transfections with several other members of the ets family, including ets-2 and fli-1, had no effect. Various mutants of PU.1 were also tested for their ability to affect macrophage proliferation. A reduction in macrophage proliferation was found when cells were transfected with a construct in which the DNA-binding domain of PU.1 was expressed. The PEST (proline-, glutamic acid-, serine-, and threonine-rich region) sequence of the PU.1 protein, which is an important domain for protein-protein interactions in B cells, was found to have no influence on PU.1-enhanced macrophage proliferation when an expression construct containing PU.1 minus the PEST domain was transfected into bone marrow-derived macrophages. In vivo, PU.1 is phosphorylated on several serine residues. The transfection of plasmids containing PU.1 with mutations at each of five serines showed that only positions 41 and 45 are critical for enhanced macrophage proliferation. We conclude that PU.1 is necessary for the M-CSF-dependent proliferation of macrophages. One of the proliferation-relevant targets of this transcription factor could be the M-CSF receptor.
Overview
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Written from the paper’s full text.
TL;DR
PU.1 is required for M-CSF-dependent macrophage proliferation: antisense PU.1 reduced proliferation, while sense PU.1 enhanced M-CSF- and GM-CSF-dependent proliferation. The effect appears linked to M-CSF receptor surface expression and requires PU.1 serine residues 41 and/or 45.
Key findings
- Antisense PU.1 expression construct or antisense oligonucleotides decreased bone marrow-derived macrophage (BMDM) proliferation; at 600 or 1,200 U/ml M-CSF, antisense versus control differences were significant (P < 0.01).
- Sense PU.1 enhanced M-CSF-dependent proliferation and also GM-CSF-dependent proliferation; the GM-CSF effect was abolished by anti-M-CSF antibodies, and anti-M-CSF caused a 30% decrease in control-vector BMDM proliferation.
- PU.1 sense increased and PU.1 antisense reduced surface M-CSF receptor expression; ets-2 and fli-1 had no effect on M-CSF-dependent proliferation.
- PU.1 mutants showed that the PEST domain was dispensable, the DNA-binding domain reduced proliferation, and only serine positions 41 and 45 were critical for enhanced macrophage proliferation.
Methods
- BMDM were obtained from 6-week-old DBA/2 mice and cultured with M-CSF/L cell-conditioned medium; macrophage cell lines RAW264.7, IC-21, and BAC1 2F5-A were also used.
- Cells were transfected by electroporation with PU.1 sense, antisense, mutant, ets-2, or fli-1 constructs, or treated with antisense oligonucleotides; transfection efficiency was 7–12% as assessed with green fluorescent protein.
- Proliferation was measured by [3H]thymidine incorporation or Coulter counting; M-CSF receptor surface expression was measured by specific antibodies and flow cytometry; experiments were performed at least five times, in triplicate, with Student’s paired t test.
Limitations
- The paper states that the number of PU.1-regulated genes that could modulate macrophage proliferation in response to M-CSF is unknown.
- Evident from the text: transfection efficiency was only 7–12%, so proliferation and receptor data reflect effects in a minority of cells within mixed populations.
- Evident from the text: some supporting results are reported as “data not shown,” including proliferation of M-CSF-independent macrophage cell lines and receptor results with antisense oligonucleotides.
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Claims the paper makes
25 Sources not found · 22 Own interpretation · 20 Own result · 5 Own method · 1 No basis given
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
“Transfection of a PU. 1 expression construct into bone marrow macrophages was found to stimulate both M- and GM-CSF-dependent pro- liferation of these cells, whereas transfection ofa PU.1 anti- sense construct or a construct that expressed DNA-binding domain of PU.1 into bone marrow macrophages was found to inhibit the proliferative effect of the growth factors.”
- Also stated in: § Results · plain
“When macrophages were transfected with an expression construct containing PU. 1, a significant increase in thymidine incorporation was observed only in cells treated with M-CSF or GM-CSF.”
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- Also stated in: § Results · plain
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
“The transfection of plasmids containing PU.1 with mutations at each of five serines showed that only positions 41 and 45 are critical for enhanced macrophage proliferation.”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Rests on an assumption: In vivo, PU.1 is phosphorylated on several serine residues.
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
“A reduction in mac- rophage proliferation was found when cells were transfected with a construct in which the DNA-binding domain of PU.1 was expressed.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Bone marrow-derived macrophages transfected with an antisense PU.1 expression construct or treated with antisense oligonucle- otides showed a decrease in proliferation compared with controls.”
- Also stated in: § Results · plain
“BMDM transfected with the antisense PU.1 construct in the presense of M-CSF had a signifi- cantly reduced thymidine incorporation compared with the controls in which the vector alone was transfected into the cells (Fig. 1 A).”
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- Also stated in: § Results · plain
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
“Transfection of PU.1 into BMDM in the absence of M-CSF had no effect on the proliferation of the macro- phages, suggesting that the effect of the antisense and sense PU. 1 constructs was growth factor dependent.”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“We observed that the antisense but not the sense oligonucle- otide inhibited BMDM thymidine incorporation in a dose- dependent manner that was dependent on the concentra- tion of M-CSF in the media (Fig. 1 B).”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The enhancement of proliferation seems to be selective for PU.1, since transfections with several other members of the ets family, including ets-2 and fli-1, had no effect.”
- Also stated in: § Results · plain
“When expression con- structs containing either ets-2 or fli-1 were transfected into BMDM, no increase in macrophage proliferation above that seen using the vector alone was detected (Fig. 6).”
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · plain
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
“When a PU. 1 expression construct lacking the PEST do- main was transfected into BMDM, an enhancement of macrophage proliferation similar to that obtained using the wild PU. 1 construction was observed”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: BMDM proliferation is a valid measure of macrophage proliferation.
- Rests on an assumption: The PU.1 constructs are expressed and function as intended in BMDM.
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
“We observed that in the presence of the mAb against M-CSF there was no stimulation ofthymidine incorporation above background when GM-CSF was added to the cultures and the PU.1 expression construct transfected into the cells (Fig. 4).”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast, bone marrow macrophages transfected with a sense PU.1 expression construct displayed enhanced macrophage colony- stimulating factor (M-CSF)-dependent proliferation.”
plaindirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 11
- Probably not a substantial claim. 24
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
“In contrast, PU.1 protein carrying an alanine substitution at $41 or $45 not only failed to stimulate pro- liferation, but also lowered the basal level of proliferation.”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Alanine substitution at serine 41 or 45 does not alter PU.1 function except by preventing phosphorylation.
- Rests on an assumption: The PU.1 constructs are expressed and function as intended in BMDM.
In the paper
“The PU.1 transcription factor in routine macrophages is known to be phosphorylated on five serines that are con- sensus sites for casein kinase II (CK II) (9, and our unpub- lished results).”
What the sources say
- Not matchedcites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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In the paper
“The PEST domain has been shown to be important for the interaction ofPU. 1 with the B cell-specific factor NF-EM5 (Pip) (8, 24).”
What the sources say
- Not matchedcites [8]
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- Not matchedcites [24]
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“A computer-assisted search of the GenBank database for mammalian sequences complementary to these anti- sense oligodeoxynucleotides revealed little homology with other genes.”
plain- Asserted: passes — The authors put it forward as true.
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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
“The decrease in proliferation observed when the DNA-binding domain was used may be due to the competiton between the endogenous PU.1 and the transfected DNA-binding domain for a target sequence in a promoter or enhancer of a gene or genes involved in pro- liferation.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Each experiment was performed at least five times and the results are expressed as the mean + SD. Statistical analyses were performed using the Student's paired t test, comparing the results of at least five independent experiments.”
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
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In the paper
“PU. 1 has been shown to bind to the promoter of the M-CSF re- ceptor and therefore may be an important factor for the regulated expression of this receptor (17, 42).”
What the sources say
- Not matchedcites [17]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [42]
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hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“PU.1 is a tissue-specific transcription factor that is expressed in cells of the hematopoietic lineage including macrophages, granulocytes, and B lymphocytes.”
- Also stated in: § Introduction · plain
“This protein is expressed in macrophages, granulocytes, mast cells, osteoclasts, and B lymphocytes (5).”
What the sources say
- Not matchedcites [4]
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- Not matchedcites [5]
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- Also stated in: § Introduction · plain
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The growth activity of LCM could be blocked by a specific mAb against M-CSF.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The amount of DNA used was 2 mg for 12 * 106 cells, which resulted in 7-12% of cells being transfected, as assessed by staining for green fluorescent protein.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A dominant negative expression construct of PU.1 in which aminos acids 133 to the end were expressed was used to show that PU. 1 was needed for expression from the J chain gene promoter (12).”
What the sources say
- Not matchedcites [12]
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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
“This latter result may be due to a general feature of the DNA-binding domains of ETS family mem- bers since dominant negative constructs of ets-1 and ets-2 had the same effect.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“In vitro, PU.1 was also shown to interact with the general transcription factor TFIID (49).”
What the sources say
- Not matchedcites [49]
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plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The infec- tion of erythroblasts with a retroviral vector expressing PU.1 was efficient for immortalization, suggesting that PU.1 perturbs the pathway that controls the potential for proliferation in these cells (48).”
What the sources say
- Not matchedcites [48]
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In the paper
“A dominant negative PU.1 expression construct (amino acids 160-266) transfected into Ras- transformed NIH3T3 fibroblasts reverted the transformed phenotype (52).”
What the sources say
- Not matchedcites [52]
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In the paper
“For instance, PU.1 binds the tumor suppressor protein p53 which represses cell proliferation (49).”
What the sources say
- Not matchedcites [49]
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plaindirect- Asserted: passes — The authors put it forward as true.
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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
“This may be due to an already high level of ets-2 expression in the cells (our unpublished results).”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Because the enhancement of proliferation requires the presence of the growth factor M-CSF, one pos- sible candidate is the M-CSF receptor (c-fms), which is spe- cifically expressed in macrophages (3).”
What the sources say
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In the paper
“The Ets family consists of a large number of proteins that have sequence identity within the DNA-binding domain, and all bind to a se- quence containing the core sequence 5'-GGAA/T-3' (43).”
What the sources say
- Not matchedcites [43]
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In the paper
“It has also been reported that ets-2 transactivates the proximal pro- moter of the M-CSF receptor (42, 53).”
What the sources say
- Not matchedcites [42]
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- Not matchedcites [53]
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The protein-protein interaction is mediated through a 43--amino acid region with sequence homology to a PEST domain, i.e., one that is rich in proline (P), glutamic acid (E), serine (S), and threonine (T), which is susceptible to protease degradation (51).”
What the sources say
- Not matchedcites [51]
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In this model, if the provirus integrates up- stream of the PU.I gene, PU.1 is overexpressed and the cell loses its commitment to terminally differentiate and be- comes immortal.”
What the sources say
- Not matchedcites [46]
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“PU.1 functions in association with other factors (8, 10, 19, 49, 50).”
What the sources say
- Not matchedcites [8]
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- Not matchedcites [10]
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- Not matchedcites [19]
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plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Mutations at this site have been shown to eliminate PU.1 binding and decrease promoter activity.”
What the sources say
- Not matchedcites [17]
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.
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In the paper
“Antisense ohgodeoxynucleotides of PU. 1 inhibit the prolif- eration of erythroleukemia cells induced by the retrovirus SFFV (46).”
What the sources say
- Not matchedcites [46]
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In the mouse, K 3' enhancer for example, PU.1 recruits a B cell-restricted factor, NF-EM5 (Pip) (8, 24).”
What the sources say
- Not matchedcites [8]
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- Not matchedcites [24]
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plaindirect- Asserted: passes — The authors put it forward as true.
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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
“PU.1 and PU.l-associated factor(s) could sta- bilize TFIID and allow assembly of the initiation complex of genes related to proliferation.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Whereas the core sequence appears to be necessary for binding it is known that flanking sequences also influence the binding of specific Ets family members to DNA (44, and our unpublished results).”
What the sources say
- Not matchedcites [44]
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: 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
The paper relies on this without support.
In vivo, PU.1 is phosphorylated on several serine residues.
“In vivo, PU. 1 is phosphorylated on several serine residues.”
The paper relies on this without support.
The macrophage cell lines IC-21, RAW264.7, and 2F5A express PU.1 endogenously.
“The prolifera- tion of three macrophage cell lines, IC-21, RAW264.7, and 2F5A, which express PU.1 endogenously, were tested using the sense and antisense constructs, and no effect on proliferation was observed (data not shown).”
The paper relies on this without support.
The cell line used to test M-CSF independence is truly M-CSF-independent.
“Interestingly, there was no effect of sense or antisense constructs of PU.1 on the proliferation of the M-CSF-independent cell line, suggesting that the response was M-CSF dependent.”
The paper relies on this without support.
The antisense and transfection experiments specifically modulate PU.1 activity without off-target effects.
“The block in macrophage prolif- eration using either an antisense PU. 1 expression construct or antisense oligonucleotides suggests that PU.1 plays a critical role in the proliferation of macrophages.”
The paper relies on this without support.
BMDM proliferation is a valid measure of macrophage proliferation.
“When a PU. 1 expression construct lacking the PEST do- main was transfected into BMDM, an enhancement of macrophage proliferation similar to that obtained using the wild PU. 1 construction was observed”
The paper relies on this without support.
Alanine substitution at serine 41 or 45 does not alter PU.1 function except by preventing phosphorylation.
“In contrast, PU.1 protein carrying an alanine substitution at $41 or $45 not only failed to stimulate pro- liferation, but also lowered the basal level of proliferation.”
The paper relies on this without support.
The PU.1 constructs are expressed and function as intended in BMDM.
“PU.1 with the $132/133A or $148A mutations was as active as the wild-type protein in stimulating proliferation of BMDM (Fig. 7 B).”
The paper relies on this without support.
The M-CSF-dependent proliferation of BMDM reflects normal macrophage proliferation.
“The enhancement of macrophage proliferation induced by the transfection of PU.1 appears to be related to the presence of M-CSF in the media.”
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
“and a PU.1 mutant at Ser-41 and -45 decreases the M-CSF-or granulocyte-macrophage colony-stimulating factor-dependent proliferation of bone marrow macrophages (54).”
From c-Jun Is a JNK-independent Coactivator of the PU.1 Transcription Factor (1999) · cites this paper as [54]
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
“phosphorylation of two serine residues (positions 41 and 45) located at one of the acidic transactivation domains is necessary for macrophage colony-stimulating factor-dependent proliferation of bone marrow macrophages (4)”
From Interleukin-3 Stimulation of mcl-1 Gene Transcription Involves Activation of the PU.1 Transcription Factor through a p38 Mitogen-Activated Protein Kinase-Dependent Pathway (2003) · cites this paper as [4]
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
“Moreover, PU.1 controls proliferation of macrophages by upregulating the receptor for M-CSF34.”
From MicroRNA-124 promotes microglia quiescence and suppresses EAE by deactivating macrophages via the C/EBP-α–PU.1 pathway (2011) · cites this paper as [34]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“and the activity of PU.1 is known to be regulated by phosphorylation (53,54,65).”
From c-Jun Is a JNK-independent Coactivator of the PU.1 Transcription Factor (1999) · cites this paper as [54]
The cited source says what the claim attributes to it.
In the citing paper
“PU.1 is known to be a vital transcription factor to regulate macrophage proliferation (54) and differentiation (55) as well as microgliogenesis (13) in the developing brain.”
From Arresting the bad seed: HDAC3 regulates proliferation of different microglia after ischemic stroke (2024) · cites this paper as [54]
In the citing paper
“In macrophages, phosphorylation of PU.1 at position Ser41 has been shown to be important for proliferation (55”
From AKT Induces Transcriptional Activity of PU.1 through Phosphorylation-mediated Modifications within Its Transactivation Domain (2001) · cites this paper as [55]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“A decrease in M-CSF-dependent proliferation, however, was observed when a PU.1 construct containing the DNA- binding domain (ETS domain) was transfected into the cells (Fig. 7 B).”
“Figure 7. (A) The DNA-binding domainofPU.1 inhibitsM-CSF--dependentproliferation.”
Citations
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“1 controls proliferation of macrophages by upregulating the receptor for M-CS”
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GM-CSF Regulates Alveolar Macrophage Differentiation and Innate Immunity in the Lung through PU.1
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“AMs are vital to normal lung PU.1 promotes both the proliferation (Celada et al., 1996)surfactant metabolism, to which they contribute by caand differentiation (DeKoter et al., 1998) of myeloid pro-tabolism of both surfactant lipids and surfactant progenitors.”
BackgroundThe AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis
Fidler, T. P., Xue, C., Yalçınkaya, M., Hardaway, B., Abramowicz, S., Xiao, T., Liu, W., Thomas, D. G., Hajebrahimi, M. A., Pircher, J., et al. (2021) · Nature · doi:10.1038/s41586-021-03341-5 · Cited by 479
Regulation of Microglial Proliferation during Chronic Neurodegeneration
Gómez-Nicola, D., Fransen, N. L., Suzzi, S., & Perry, V. H. (2013) · The Journal of Neuroscience · doi:10.1523/jneurosci.4440-12.2013 · Cited by 407
“PU.1 is a master regulator of myeloid differentiation and induces the expression of CD45, CD11b, F4/ 80, and MHC class II as well as regulating cell proliferation by upregulating the CSF1R (Celada et al., 1996; Nishiyama et al., 2004).”
BackgroundTrapnell, B. C., & Whitsett, J. A. (2002) · Annual Review of Physiology · doi:10.1146/annurev.physiol.64.090601.113847 · Cited by 353
Diseases of Pulmonary Surfactant Homeostasis
Whitsett, J. A., Wert, S. E., & Weaver, T. E. (2015) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-012513-104644 · Cited by 256
Transcription factors that regulate monocyte/macrophage differentiation
Valledor, A. F., Borràs, F. E., Cullell-Young, M., & Celada, A. (1998) · Journal of Leukocyte Biology · doi:10.1002/jlb.63.4.405 · Cited by 215
“1 increased the M-CSF-dependent proliferation of these cells [12].”
BackgroundSelf-citationRegulation of interleukin-12 production in antigen-presenting cells
Mal, X., & Trinchieri, G. (2001) · Advances in immunology · doi:10.1016/s0065-2776(01)79002-5 · Cited by 213
OxInflammation: From Subclinical Condition to Pathological Biomarker
Valacchi, G., Virgili, F., Cervellati, C., & Pecorelli, A. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00858 · Cited by 212
“It is well known that these factors are master regulators of genes associated with differentiation, proliferation, and migration of immune cells and resident vascular cells, and modulate the expression of a plethora of proinflammatory and immune factors (Celada et al., 1996).”
BackgroundLiu, J., Cao, S., Kim, S. J., Chung, E. Y., Homma, Y., Guan, X., Jimenez, V., & Ma, X. (2005) · Current Immunology Reviews · doi:10.2174/1573395054065115 · Cited by 189
“It is expressed predominantly in macrophages, B-cells, and erythroid cells [179,180].”
BackgroundNutma, E., Fancy, N. N., Weinert, M., Tsartsalis, S., Marzin, M. C., Muirhead, R. C. J., Falk, I. N., Breur, M., de Bruin, J., Hollaus, D., et al. (2023) · Nature Communications · doi:10.1038/s41467-023-40937-z · Cited by 197
“The PU.1 transcription factor is a master regulator of macrophage proliferation and macrophage differentiation 32,33 .”
c-Jun Is a JNK-independent Coactivator of the PU.1 Transcription Factor
Behre, G., Whitmarsh, A. J., Coghlan, M. P., Hoang, T., Carpenter, C. L., Zhang, D.-E., Davis, R. J., & Tenen, D. G. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.8.4939 · Cited by 180
ETS transcription factors and regulation of immunity
Gallant, S., & Gilkeson, G. S. (2006) · Archivum Immunologiae et Therapiae Experimentalis · doi:10.1007/s00005-006-0017-z · Cited by 165
“1 levels directly impacts M-CSF-dependent proliferation of macrophages and myeloid progenitors [25, 33, 140, 197].”
BackgroundFisher, R. C., & Scott, E. W. (1998) · STEM CELLS · doi:10.1002/stem.160025 · Cited by 158
Reddy, V. A., Iwama, A., Iotzova, G., Schulz, M., Elsasser, A., Vangala, R. K., Tenen, D. G., Hiddemann, W., & Behre, G. (2002) · Blood · doi:10.1182/blood.v100.2.483 · Cited by 152
Autophagy Driven by a Master Regulator of Hematopoiesis
Kang, Y.-A., Sanalkumar, R., O'Geen, H., Linnemann, A. K., Chang, C.-J., Bouhassira, E. E., Farnham, P. J., Keles, S., & Bresnick, E. H. (2012) · Molecular and Cellular Biology · doi:10.1128/mcb.06166-11 · Cited by 153
“Genome-wide studies of GATA-1 chromatin occupancy have analyzed endogenous GATA-1 in K562 erythroleukemia cells (9) and biotinylated GATA-1 in MEL cells (5, 56).”
BackgroundThe key role of PU.1/SPI-1 in B cells, myeloid cells and macrophages
Lloberas, J., Soler, C., & Celada, A. (1999) · Immunology Today · doi:10.1016/s0167-5699(99)01442-5 · Cited by 142
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“1 [42, 43], which is a tissuespecific transcription factor, resulting in the downregulation of the Toll-like receptor 4 (TLR4) expression [44].”
BackgroundValledor, A. F., Comalada, M., Xaus, J., & Celada, A. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.10.7403 · Cited by 135
Self-citationRegulation of granulopoiesis by transcription factors and cytokine signals
Ward, A. C., Loeb, D., Soede-Bobok, A. A., Touw, I., & Friedman, A. (2000) · Leukemia · doi:10.1038/sj.leu.2401808 · Cited by 134
Molecular Mechanisms Involved in Macrophage Survival, Proliferation, Activation or Apoptosis
Xaus, J., Comalada, M., Valledor, A. F., Cardó, M., Herrero, C., Soler, C., Lloberas, J., & Celada, A. (2001) · Immunobiology · doi:10.1078/0171-2985-00091 · Cited by 130
Self-citationXaus, J., Comalada, M., Cardó, M., Valledor, A. F., & Celada, A. (2001) · Blood · doi:10.1182/blood.v98.7.2124 · Cited by 129
Self-citationMicroglia: unique and common features with other tissue macrophages
Prinz, M., Tay, T. L., Wolf, Y., & Jung, S. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1267-1 · Cited by 126
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The JNK Are Important for Development and Survival of Macrophages
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“1 transcription factor has been shown to effect proliferation of BMMs in a CSF-1-dependent manner, and decreased proliferation of BMMs in response to JNK inhibition may partially occur through repression of c-fms gene expression (54) (Fig.”
BackgroundLau, S.-F., Chen, C., Fu, W.-Y., Qu, J. Y., Cheung, T. H., Fu, A. K. Y., & Ip, N. Y. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.107530 · Cited by 114
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Comalada, M., Xaus, J., Valledor, A. F., López, C., Pennington, D. J., & Celada, A. (2003) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00228.2003 · Cited by 109
“Because these cells cannot be transfected efficiently, we used specific chemical inhibitors (12).”
MethodSelf-citationSmith, A. M., Gibbons, H. M., Oldfield, R. L., Bergin, P. M., Mee, E. W., Curtis, M. A., Faull, R. L. M., & Dragunow, M. (2013) · Journal of Neuroinflammation · doi:10.1186/1742-2094-10-85 · Cited by 107
“1 has been shown to be involved in M-CSF -dependent proliferation of mouse bone-marrow macrophages [24] and thus it is likely that PU.”
BackgroundInfluentialOverexpression of sphingosine kinase 1 is an oncogenic event in erythroleukemic progression
Scolan, E. L., Pchejetski, D., Banno, Y., Denis, N., Mayeux, P., Vainchenker, W., Levade, T., & Moreau-Gachelin, F. (2005) · Blood · doi:10.1182/blood-2004-12-4832 · Cited by 110
Development and function of tissue resident macrophages in mice
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Selective Roles of MAPKs during the Macrophage Response to IFN-γ
Valledor, A. F., Sànchez‐Tilló, E., Arpa, L., Park, J. M., Caelles, C., Lloberas, J., & Celada, A. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.180.7.4523 · Cited by 97
“For our studies, we used homogeneous populations of primary bone marrow-derived macrophages, which become activated under the effect of IFN- (11, 20).”
MethodSelf-citationSuppression of IL-12 Transcription in Macrophages Following Fcγ Receptor Ligation
Cappiello, M. G., Sutterwala, F. S., Trinchieri, G., Mosser, D. M., & Ma, X. (2001) · The Journal of Immunology · doi:10.4049/jimmunol.166.7.4498 · Cited by 98
“It is expressed predominantly in macrophages, B cells, and erythroid cells (27, 28).”
BackgroundShort telomeres protect from diet‐induced atherosclerosis in apolipoprotein E‐null mice
Poch, E., Carbonell, P., Franco, S., Díez‐Juan, A., Blasco, M. A., & Andrés, V. (2003) · The FASEB Journal · doi:10.1096/fj.03-0710fje · Cited by 94
“Splenocytes and bone marrow-derived macrophages were obtained from the pooled tissue from three mice as described previously (28, 33).”
MethodYeramian, A., Jaular, L. M., Arpa, L., Bertran, J., Soler, C., McLeod, C., Modolell, M., Palacı́n, M., Lloberas, J., & Celada, A. (2006) · European Journal of Immunology · doi:10.1002/eji.200535694 · Cited by 91
Self-citationSebastián, C., Herrero, C., Serra, M., Lloberas, J., Blasco, M. A., & Celada, A. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0901131 · Cited by 94
“Macrophage proliferation was measured by [(3)H]thymidine incorporation as described (11).”
MethodSelf-citationWang, J.-M., Lai, M.-Z., & Yang-Yen, H.-F. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.6.1896-1909.2003 · Cited by 90
“While phosphorylation of two serine residues (positions 41 and 45) located at one of the acidic transactivation domains is necessary for macrophage colony-stimulating factor-dependent proliferation of bone marrow macrophages (4), a serine phosphorylation at position 148 in the proline-, glutamic-acid-, serine-, and th…”
BackgroundXaus, J., Valledor, A. F., Cardó, M., Marqués, L., Beleta, J., Palacios, J. M., & Celada, A. (1999) · The Journal of Immunology · doi:10.4049/jimmunol.163.8.4140 · Cited by 83
“In this report, we have used primary cultures of BMDM, which is an homogeneous population that responds to physiological proliferative or activating stimuli (54).”
MethodSelf-citationPU.1 but not ets-2 is essential for macrophage development from embryonic stem cells
Henkel, G., McKercher, Sr., Yamamoto, H., Anderson, K., Oshima, R., & Maki, R. (1996) · Blood · doi:10.1182/blood.v88.8.2917.bloodjournal8882917 · Cited by 76
Self-citationPU.1/Interferon Regulatory Factor Interactions; Mechanisms of Transcriptional Regulation
Marecki, S., & Fenton, M. J. (2000) · Cell Biochemistry and Biophysics · doi:10.1385/cbb:33:2:127 · Cited by 74
“In some instances, binding of both factors to DNA is required; in others, PU.1 may actually tether another factor to the DNA, as has been reported for c-Jun on the M-CSF promoter and C/EBPβ on the IL-1β promoter (35,36).”
BackgroundInfluentialValledor, A. F., Xaus, J., Marqués, L., & Celada, A. (1999) · The Journal of Immunology · doi:10.4049/jimmunol.163.5.2452 · Cited by 74
Self-citationWalton, M. R., Gibbons, H., MacGibbon, G. A., Sirimanne, E., Saura, J., Gluckman, P. D., & Dragunow, M. (2000) · Journal of Neuroimmunology · doi:10.1016/s0165-5728(99)00262-3 · Cited by 73
Decorin Reverses the Repressive Effect of Autocrine-Produced TGF-β on Mouse Macrophage Activation
Comalada, M., Cardó, M., Xaus, J., Valledor, A. F., Lloberas, J., Ventura, F., & Celada, A. (2003) · The Journal of Immunology · doi:10.4049/jimmunol.170.9.4450 · Cited by 68
“Bone marrow-derived macrophages were isolated from 6-wk-old BALB/c mice (Charles River Laboratories, Wilmington, MA) as previously described (16).”
MethodSelf-citationReview: The Role of IRF-4 in Transcriptional Regulation
Marecki, S., & Fenton, M. J. (2002) · Journal of Interferon & Cytokine Research · doi:10.1089/107999002753452737 · Cited by 68
“(63,64) Importantly, serine 148 phosphorylation is required to enhance protein-protein interaction with IRF-4 or with ICSBP/IRF-8.”
MicroRNAs in the Brain: It's Regulatory Role in Neuroinflammation
Thounaojam, M. C., Kaushik, D. K., & Basu, A. (2013) · Molecular Neurobiology · doi:10.1007/s12035-013-8400-3 · Cited by 66
“1 is a master regulator of macrophage cell differentiation and proliferation that play a crucial role in the activation of the phenotype of monocytic lineage [42].”
BSAP Can Repress Enhancer Activity by Targeting PU.1 Function
Maitra, S., & Atchison, M. L. (2000) · Molecular and Cellular Biology · doi:10.1128/mcb.20.6.1911-1922.2000 · Cited by 64
“1 is known to influence macrophage proliferation (5), BSAP expression in early B-cell precursors could limit the expansion of cells into the myeloid pathway by inhibiting PU.”
BackgroundBellón, T., Perrotti, D., & Calabretta, B. (1997) · Blood · doi:10.1182/blood.v90.5.1828 · Cited by 62
Sànchez‐Tilló, E., Comalada, M., Xaus, J., Farrera, C., Valledor, A. F., Caelles, C., Lloberas, J., & Celada, A. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m609662200 · Cited by 61
Self-citationSierra, S., Lara‐Villoslada, F., Comalada, M., Olivares, M. M., & Xaus, J. (2006) · Lipids · doi:10.1007/s11745-006-5061-2 · Cited by 62
Luo, Q., Ma, X., Wahl, S. M., Bieker, J. J., Crossley, M., & Montaner, L. J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m400320200 · Cited by 59
Arresting the bad seed: HDAC3 regulates proliferation of different microglia after ischemic stroke
Zhang, Y., Li, J., Zhao, Y., Huang, Y., Shi, Z., Wang, H., Cao, H., Wang, C., Wang, Y., Chen, D., et al. (2024) · Science Advances · doi:10.1126/sciadv.ade6900 · Cited by 55
“PU.1 is known to be a vital transcription factor to regulate macrophage proliferation ( 54 ) and differentiation ( 55 ) as well as microglio-genesis ( 13 ) in the developing brain.”
BackgroundComalada, M., Xaus, J., Sànchez‐Tilló, E., Valledor, A. F., & Celada, A. (2004) · European Journal of Immunology · doi:10.1002/eji.200425110 · Cited by 57
Self-citationLiu, J., & Ma, X. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m602059200 · Cited by 56
Evidence of recent signatures of selection during domestication in an Atlantic salmon population
Gutiérrez, A. P., Yañez, J. M., & Davidson, W. S. (2015) · Marine Genomics · doi:10.1016/j.margen.2015.12.007 · Cited by 56
“1, a transcription factor linked to macrophage proliferation (Celada et al., 1996), ESTV_12965_608 is associatedwith Sema6d a genewith a role in immune response and development (Vadasz and Toubi, 2014) and ESTV_16140_475 is associated with prothymosin α that has an immunoregulatory role during infection (Shiau et al.”
BackgroundSebastián, C., Serra, M., Yeramian, A., Serrat, N., Lloberas, J., & Celada, A. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.180.9.5898 · Cited by 54
“Macrophage proliferation was measured by [(3)H]thymidine incorporation as described (26).”
MethodSelf-citationRieske, P., & Pongubala, J. R. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m007482200 · Cited by 54
Wontakal, S. N., Guo, X., Will, B., Shi, M., Raha, D., Mahajan, M. C., Weissman, S., Snyder, M., Steidl, U., Zheng, D., et al. (2011) · PLoS Genetics · doi:10.1371/journal.pgen.1001392 · Cited by 53
“1 has been reported to promote proliferation of both erythroid progenitors [10,43] and bone marrow derived macrophages [73].”
BackgroundGangenahalli, G. U., Gupta, P., Saluja, D., Verma, Y. K., Kishore, V., Chandra, R., Sharma, R. K., & Ravindranath, T. (2005) · Stem Cells and Development · doi:10.1089/scd.2005.14.140 · Cited by 53
“Bone marrow derived-macrophages transfected with an antisense PU.1 construct showed reduced proliferation as compared with controls, whereas those transfected with sense PU.1 construct displayed enhanced M-CSF-dependent proliferation (49).”
Quang, C. T., Wessely, O., Pironin, M., Beug, H., & Ghysdael, J. (1997) · The EMBO Journal · doi:10.1093/emboj/16.18.5639 · Cited by 54
“…express high levels of Spi-1/PU.1 and require in the primary leukemic cells from which they were derived (Mowat et al., 1985; Chow et al., 1987; Ben-Davidthis transcription factor for their normal development (Scott et al., 1994; Celada et al., 1996; McKercher et al., 1990; Munroe et al., 1990).”
BackgroundCommitment to the Monocytic Lineage Occurs in the Absence of the Transcription Factor PU.1
Henkel, G. W., McKercher, S. R., Leenen, P. J. M., & Maki, R. A. (1999) · Blood · doi:10.1182/blood.v93.9.2849 · Cited by 53
Self-citationMicroRNAs as Novel Regulators of Neuroinflammation
Ksiazek-Winiarek, D. J., Kacperska, M. J., & Glabinski, A. R. (2013) · Mediators of Inflammation · doi:10.1155/2013/172351 · Cited by 51
“1 plays important role in the activation of monocytic lineage phenotype [117].”
BackgroundNBS1 is required for macrophage homeostasis and functional activity in mice
Pereira‐Lopes, S., Tur, J., Calatayud-Subias, J. A., Lloberas, J., Stracker, T. H., & Celada, A. (2015) · Blood · doi:10.1182/blood-2015-04-637371 · Cited by 53
“BM-derived macrophages (BMDMs) were generated as described.(21) A homogeneous populationof adherentmacrophageswasobtainedafter 7 daysof culture (.”
MethodInfluentialSelf-citationFisher, R. C., Olson, M. C., Pongubala, J. M. R., Perkel, J. M., Atchison, M. L., Scott, E. W., & Simon, M. C. (1998) · Molecular and Cellular Biology · doi:10.1128/mcb.18.7.4347 · Cited by 49
“1 activation domain have been implicated in the M-CSF-dependent proliferation of murine bone marrow macrophages (4).”
BackgroundMonocyte depletion increases local proliferation of macrophage subsets after skeletal muscle injury
Côt́e, C. H., Bouchard, P., van Rooijen, N., Marsolais, D., & Duchesne, É. (2013) · BMC Musculoskeletal Disorders · doi:10.1186/1471-2474-14-359 · Cited by 51
“This is in accordance with the reported proliferative ability of a number of macrophage subtypes including macrophages located in brain [35,37] or peritoneum [38], bone marrow-derived macrophages in culture [39], and the macrophage cell line RAW-264.”
ResultThe ETS Family of Transcriptional Regulators
Ghysdael, J., & Boureux, A. (1997) · Birkhäuser Basel eBooks · doi:10.1007/978-3-0348-8889-9_2 · Cited by 48
Valproic acid induces microglial dysfunction, not apoptosis, in human glial cultures
Gibbons, H. M., Smith, A. M., Teoh, H. H., Bergin, P. M., Mee, E. W., Faull, R. L. M., & Dragunow, M. (2011) · Neurobiology of Disease · doi:10.1016/j.nbd.2010.08.024 · Cited by 49
Casals‐Casas, C., Álvarez, E., Serra, M., de la Torre, C., Farrera, C., Sànchez‐Tilló, E., Caelles, C., Lloberas, J., & Celada, A. (2009) · European Journal of Immunology · doi:10.1002/eji.200839037 · Cited by 48
Self-citationCasals, C., Barrachina, M., Serra, M., Lloberas, J., & Celada, A. (2007) · The Journal of Immunology · doi:10.4049/jimmunol.178.10.6307 · Cited by 48
Self-citationValledor, A. F., Arpa, L., Sànchez‐Tilló, E., Comalada, M., Casals, C., Xaus, J., Caelles, C., Lloberas, J., & Celada, A. (2008) · Blood · doi:10.1182/blood-2007-11-123604 · Cited by 48
Self-citationRao, S., Matsumura, A., Yoon, J. W., & Simon, M. C. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.16.11115 · Cited by 46
Kim, J., Kim, H., Kwon, S. B., Lee, S. Y., Chung, S., Jeong, D., & Min, B. (2004) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2004.09.220 · Cited by 47
Tsubakimoto, Y., Yamada, H., Yokoi, H., Kishida, S., Takata, H., Kawahito, H., Matsui, A., Urao, N., Nozawa, Y., Hirai, H., et al. (2009) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.109.187732 · Cited by 47
Jones, R. E., Andrews, R., Holmans, P., Hill, M., & Taylor, P. R. (2021) · Scientific Reports · doi:10.1038/s41598-021-94324-z · Cited by 39
Hafez, H. A., Kamel, M. A. E.-N., Osman, M. Y. H., Osman, H., Elblehi, S. S., & Mahmoud, S. A. (2021) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-021-04079-4 · Cited by 42
Origins of lymphocyte developmental programs: transcription factor evidence
Rothenberg, E. V., & Pant, R. (2004) · Seminars in Immunology · doi:10.1016/j.smim.2004.08.002 · Cited by 42
Quantitative Proteomic Characterization of Ethanol-Responsive Pathways in Rat Microglial Cells
Bell‐Temin, H., Zhang, P., Chaput, D., King, M. A., You, M., Liu, B., & Stevens, S. M. (2013) · Journal of Proteome Research · doi:10.1021/pr301038f · Cited by 43
López‐Rodríguez, C., & Corbí, A. L. (1997) · European Journal of Immunology · doi:10.1002/eji.1830270804 · Cited by 36
Bush, S. J., Freem, L. J., MacCallum, A. J., O’Dell, J., Wu, C., Afrasiabi, C., Psifidi, A., Stevens, M. P., Smith, J., SUMMERS, K. M., et al. (2018) · BMC Genomics · doi:10.1186/s12864-018-4972-7 · Cited by 40
IL‐4 blocks M‐CSF‐dependent macrophage proliferation by inducing p21Waf1 in a STAT6‐dependent way
Arpa, L., Valledor, A. F., Lloberas, J., & Celada, A. (2009) · European Journal of Immunology · doi:10.1002/eji.200838283 · Cited by 39
Self-citationProtein Acetylation Regulates Both PU.1 Transactivation and Igκ 3′ Enhancer Activity
Bai, Y., Srinivasan, L., Perkins, L., & Atchison, M. L. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.175.8.5160 · Cited by 39
Choe, K. S., Ujhelly, O., Wontakal, S. N., & Skoultchi, A. I. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.077727 · Cited by 38
Hematopoietic stem cells and retroviral infection
Banerjee, P., Crawford, L. B., Samuelson, E., & Feuer, G. (2010) · Retrovirology · doi:10.1186/1742-4690-7-8 · Cited by 42
“1 expression results not only in the loss of B-cells and macrophage development, but also delays T lymphopoiesis [143,144].”
BackgroundIglesias–Ara, A., Zenarruzabeitia, O., Fernández‐Rueda, J., Sànchez‐Tilló, E., Field, S. J., Celada, A., & Zubiaga, A. M. (2010) · Oncogene · doi:10.1038/onc.2010.296 · Cited by 32
Self-citationPascual-García, M., Carbo, J. M. C. I., León, T. E., Matalonga, J., Out, R., van Berkel, T. J. C., Sarrias, M., Lozano, F., Celada, A., & Valledor, A. F. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1000585 · Cited by 35
“Cell proliferation was measured as previously described (31), with minor modifications.”
MethodSelf-citationETS Transcription Factors in Immune Cells and Immune-Related Diseases
Yang, Y., Han, X., Sun, L., Shao, F., Yin, Y., & Zhang, W. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms251810004 · Cited by 37
Taming of macrophage and microglial cell activation by microRNA-124
Conrad, A., & Dittel, B. N. (2011) · Cell Research · doi:10.1038/cr.2011.9 · Cited by 29
Sànchez‐Tilló, E., Comalada, M., Farrera, C., Valledor, A. F., Lloberas, J., & Celada, A. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.176.11.6594 · Cited by 30
“siRNA were obtained from Dharmacon and transfected by electroporation (31).”
Self-citationGuerrero‐Carrasco, M., Targett, I. L., Olmos‐Alonso, A., Vargas‐Caballero, M., & Gómez‐Nicola, D. (2024) · Glia · doi:10.1002/glia.24532 · Cited by 27
“Research using hematopoietic stem cells has shown that inflammatory cytokines, such as IL-1 β and TNF α , can upregulate the expression of Pu.1 (Etzrodt et al., 2019), a transcription factor that can control microglial proliferation by stimulating Csf1r expression (Celada et al., 1996).”
BackgroundPhosphatidylinositol 4-phosphatase type II is an erythropoietin-responsive gene
Barnache, S., Scolan, E. L., Kosmider, O., Denis, N., & Moreau-Gachelin, F. (2005) · Oncogene · doi:10.1038/sj.onc.1209187 · Cited by 26
“Spi-1/PU.1 is a master gene in the development of B lymphoid, monocyte and neutrophilic lineages (Scott et al., 1994; Celada et al., 1996; Oikawa et al., 1999).”
BackgroundPU.1 as a chromatin accessibility factor for immunoglobulin genes
Marecki, S., McCarthy, K. M., & Nikolajczyk, B. S. (2004) · Molecular Immunology · doi:10.1016/j.molimm.2003.08.007 · Cited by 25
Macrophage inflammation resolution requires CPEB4-directed offsetting of mRNA degradation
Suñer, C., Sibilio, A., Martín, J., et al. (2022) · eLife · doi:10.7554/elife.75873 · Cited by 24
Comalada, M., Valledor, A. F., Sànchez‐Tilló, E., Umbert, I. J., Xaus, J., & Celada, A. (2003) · European Journal of Immunology · doi:10.1002/eji.200324074 · Cited by 24
Self-citationThe Exercise Training Modulatory Effects on the Obesity-Induced Immunometabolic Dysfunctions
Soltani, N., Marandi, S. M., Kazemi, M., & Esmaeil, N. (2020) · Diabetes Metabolic Syndrome and Obesity · doi:10.2147/dmso.s234992 · Cited by 27
“MФs, then, possess a larger periphery, longer lifetime (up to several months), and more phagocytic features than MONs.69 Nevertheless, MONs which do not migrate into the tissues (in order not to participate in an immunity response) will die after these few days.37 They initially act as environmental sensors and also p…”
BackgroundPU.1 Regulates Cathepsin S Expression in Large Yellow Croaker (Larimichthys crocea) Macrophages
Zhang, X.-Y., Zhuo, X., Cheng, J., Wang, X., Liang, K., & Chen, X. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2021.819029 · Cited by 21
“The transactivation domain is required for the M-CSF-dependent proliferation of macrophages (23).”
BackgroundInfluentialHematopoietic Stem Cell Molecular Targets and Factors Essential for Hematopoiesis
Raghav, P. K., & Gangenahalli, G. U. (2018) · Journal of Stem Cell Research & Therapy · doi:10.4172/2157-7633.1000441 · Cited by 22
“In the PEST domain, residues 41 and 45 are essential for the enhancement of macrophage proliferation [50].”
Background
Metadata
- Authors
- Celada, A., Borràs, F. E., Soler, C., Lloberas, J., Klemsz, M., van Beveren, C., McKercher, S., & Maki, R. A.
- Affiliations
- Universitat de Barcelona (ES)
- Departament de Fisiologia (Immunologia), Facultat de Biologia, Universitat de Barcelona, Spain.
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1996-07-01
- Volume
- 184
- Issue
- 1
- Pages
- 61-69
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2192661
- OpenAlex
- W1972310581
- Cited by
- 152
- References
- 59
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 7 · 2023: 3 · 2022: 13 · 2021: 5 · 2020: 4 · 2019: 1 · 2018: 4 · 2017: 1 · 2016: 1 · 2015: 6 · 2014: 1 · 2013: 7
- FWCI
- 2.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (submittedVersion, public-domain)
- Funders
- National Cancer Institute (R01CA042909)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Keywords
- PU.1, macrophage proliferation, macrophage colony-stimulating factor, M-CSF receptor, transcription factors, ETS family, ETS2, FLI1, DNA-binding domain, PEST domain, serine phosphorylation, bone marrow-derived macrophages, hematopoietic lineage
- MeSH terms
- Proto-Oncogene Protein Spi-1, Animals, Base Sequence, Bone Marrow Cells, DNA-Binding Proteins, Gene Expression Regulation, Macrophage Activation, Macrophages, Mice, Inbred DBA, Molecular Sequence Data, Proto-Oncogene Proteins, Trans-Activators, Macrophage Colony-Stimulating Factor, Granulocyte-Macrophage Colony-Stimulating Factor, DNA, Antisense, Mice
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