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
Cites
Green fluorescent protein as a marker for gene expression
Chalfie, M., Tu, Y., Euskirchen, G., Ward, W. W., & Prasher, D. C. (1994) · Science · doi:10.1126/science.8303295 · Cited by 6,802 · cited 1×
“After 2 d of culture, cells were fixed, stained, and counted (29).”
BackgroundAmino Acid Sequences Common to Rapidly Degraded Proteins: The PEST Hypothesis
Rogers, S. W., Wells, R., & Rechsteiner, M. (1986) · Science · doi:10.1126/science.2876518 · Cited by 2,541 · cited 1×
“, one that is rich in proline (P), glutamic acid (E), serine (S), and threonine (T), which is susceptible to protease degradation (51).”
BackgroundLuckow, B., & Schütz, G. (1987) · Nucleic Acids Research · doi:10.1093/nar/15.13.5490 · Cited by 1,650
Requirement of transcription factor PU.1 in the development of multiple hematopoietic lineages
Scott, E. W., Simon, M. C., Anastasi, J., & Singh, H. (1994) · Science · doi:10.1126/science.8079170 · Cited by 1,532 · cited 1×
“(25) have reported the absence o f h o m o zygous mutant progeny, suggesting that disruption o f PU.”
BackgroundEllis, L., Clauser, E., Morgan, D. O., Edery, M., Roth, R. A., & Rutter, W. J. (1986) · Cell · doi:10.1016/0092-8674(86)90786-5 · Cited by 1,070
Metcalf, D. (1989) · Nature · doi:10.1038/339027a0 · Cited by 1,023
The macrophage and B cell-specific transcription factor PU.1 is related to the ets oncogene
Klemsz, M. J., McKercher, S. R., Celada, A., Van Beveren, C., & Maki, R. A. (1990) · Cell · doi:10.1016/0092-8674(90)90219-5 · Cited by 954
Self-citationGene inhibition using antisense oligodeoxynucleotides
Wagner, R. W. (1994) · Nature · doi:10.1038/372333a0 · Cited by 747 · cited 1×
“into the functional importance of a variety of genes (45).”
BackgroundGunning, P. W., Leavitt, J. C., Muscat, G. E. O., Ng, S. Y., & Kedes, L. (1987) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.84.14.4831 · Cited by 739 · cited 1×
“I cDNA into the HindlII - Sal sites of the pHb APr-l-neo vector in the reverse orientation (32).”
MethodPhysicochemical properties of phospborothioate oligodeoxynucleotides
Stein, C. A., Subasinghe, C., Shinozuka, K., & Cohen, J. S. (1988) · Nucleic Acids Research · doi:10.1093/nar/16.8.3209 · Cited by 593
Cited by
Sorted by citations
Pulmonary Alveolar Proteinosis
Trapnell, B. C., Whitsett, J. A., & Nakata, K. (2003) · New England Journal of Medicine · doi:10.1056/nejmra023226 · Cited by 790
Ponomarev, E. D., Veremeyko, T., Barteneva, N., Krichevsky, A. M., & Weiner, H. L. (2011) · Nature Medicine · doi:10.1038/nm.2266 · Cited by 787
“1 controls proliferation of macrophages by upregulating the receptor for M-CS”
Pulmonary Alveolar Proteinosis: Progress in the First 44 Years
Seymour, J. F., & Presneill, J. (2002) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.2109105 · Cited by 694
Transcription Factors, Normal Myeloid Development, and Leukemia
Tenen, D. G., Hromas, R., Licht, J. D., & Zhang, D.-E. (1997) · Blood · doi:10.1182/blood.v90.2.489 · Cited by 735
GM-CSF Regulates Alveolar Macrophage Differentiation and Innate Immunity in the Lung through PU.1
Shibata, Y., Berclaz, P., Chroneos, Z. C., Yoshida, M., Whitsett, J. A., & Trapnell, B. C. (2001) · Immunity · doi:10.1016/s1074-7613(01)00218-7 · Cited by 623
“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.”
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-07, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-07 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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