The DOI matches its Crossref record; 62 of the 64 references it cites were found in a registry or an index; 22 of the 49 sources its claims cite were checked for support.
Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers
Open accessAbstract
Gene expression in higher eukaryotes appears to be regulated by specific combinations of transcription factors binding to regulatory sequences. The Ets factor PU.1 and the IRF protein Pip (IRF-4) represent a pair of interacting transcription factors implicated in regulating B cell-specific gene expression. Pip is recruited to its binding site on DNA by phosphorylated PU.1. PU.1-Pip interaction is shown to be template directed and involves two distinct protein-protein interaction surfaces: (i) the ets and IRF DNA-binding domains; and (ii) the phosphorylated PEST region of PU.1 and a lysine-requiring putative alpha-helix in Pip. Thus, a coordinated set of protein-protein and protein-DNA contacts are essential for PU.1-Pip ternary complex assembly. To analyze the function of these factors in vivo, we engineered chimeric repressors containing the ets and IRF DNA-binding domains connected by a flexible POU domain linker. When stably expressed, the wild-type fused dimer strongly repressed the expression of a rearranged immunoglobulin lambda gene, thereby establishing the functional importance of PU.1-Pip complexes in B cell gene expression. Comparative analysis of the wild-type dimer with a series of mutant dimers distinguished a gene regulated by PU.1 and Pip from one regulated by PU.1 alone. This strategy should prove generally useful in analyzing the function of interacting transcription factors in vivo, and for identifying novel genes regulated by such complexes.
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Claims the paper makes
96 Own result · 71 Own interpretation · 18 Own method · 15 No full text of the sources · 10 Supported · 8 Partly supported · 4 No basis given · 3 Sources not found · 3 Not checked yet · 2 Couldn’t confirm · 1 Supported so far · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“When co-expressed ectopically, PU.1 and Pip synergistically activate transcription of a reporter gene containing multiple copies of the composite element from the IgL λ enhancer, E λ2-4 (Eisenbeis et al., 1995).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Introduction
What the sources say
- Supportedcites Eisenbeis et al., 1995 source
The section “In conjunction with PU.1, Pip functions as a transcriptional activator” reports that neither protein alone activated the reporter, whereas co-expression in NIH-3T3 cells did. Figure 6 identifies the reporter as containing a tetramer of composite elements from the Eλ2-4 enhancer. (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A C-terminal regulatory domain within Pip itself is also required for ternary complex assembly (Brass et al., 1996).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Introduction
What the sources say
- Partly supportedcites Brass et al., 1996 sourceExperimental — accuracy not yet measured
The deletion analysis reports that Pip amino acids 410–439 are necessary for high-affinity ternary complex formation with PU.1. However, mutants lacking that segment still formed weak ternary complexes, so the paper does not show that the C-terminal domain is required for assembly altogether. The relevant passages are in the section on Pip repression of IFN-inducible transcription; page numbers are unavailable in our copy. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In addition, this regulatory domain autoinhibits binding of Pip to DNA in the absence of PU.1.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Introduction
What the sources say
- Supportedcites Brass et al., 1996 source
The 'Structural basis for PU.1-dependent DNA-binding of Pip' section identifies amino acids 138–450 as a regulatory domain responsible for autoinhibition of DNA binding. The deletion-analysis section reports that full-length Pip did not bind DNA independently but formed a ternary complex with PU.1. Page numbers are not provided in the supplied passages. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Previously, using deletion analysis and secondary structure predictions, we suggested that a putative α-helical region (amino acids 399-413) in Pip's C-terminus is important for ternary complex formation with PU.1 (Figure 1A and B; Brass et al., 1996).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
What the sources say
- Supportedcites Brass et al., 1996 source
In “Structural basis for PU.1-dependent DNA-binding of Pip,” the authors predict an α-helical region in Pip’s C-terminus and postulate that it may play a key role in ternary complex formation. The “Model of PU.1/Pip ternary complex formation” identifies that putative helix as amino acids 399–413. The citing sentence preserves the paper’s tentative framing. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“PU.1 and Pip represent the major components of the ternary complex formed with nuclear extract from these cells”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > The PipPU chimeric repressor blocks endogenous IgL λ gene expression when stably expressed in B cells
What the sources say
- Supportedcites Brass et al., 1996 source
In the “Pip is NF-EM5” section (page not provided), anti-PU.1 and anti-Pip antisera each supershift the JB2 complex formed with J558L nuclear extract. The authors conclude that Pip is the predominant factor associating with PU.1 on these enhancer segments in J558L cells. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“On lower affinity sites, however, the chelating effect provided by the linker may lower the overall entropic cost associated with binding, allowing PipPU to bind as efficiently as the wildtype proteins”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
What the sources say
- Partly supportedcites Klemm and Pabo, 1996 sourceExperimental — accuracy not yet measured
The “Contribution of the linker to cooperative binding” section (page unavailable) says the linker produces a chelate effect and reduces the entropic cost of complex formation. The paper studies Oct-1 POU-domain binding; it does not establish that PipPU binds lower-affinity sites as efficiently as wild-type proteins. (LLM, conf=0.87)
hedgedconditional- 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“it appears that other, as yet uncharacterized helices within this region may pack together with Pip's helix amino acids 395-413 to form a tertiary fold which is competent for PU.1 association.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
What the sources say
- Partly supportedcites Brass et al., 1996 sourceExperimental — accuracy not yet measured
In the deletion-analysis passage (page not available), removing Pip residues 150–340 weakened ternary complex formation with PU.1; the authors suggest that region may position the carboxy-terminal domain or contain another required region. In “Structural basis for PU.1-dependent DNA-binding of Pip” (page not available), they propose a role for a putative helix near residues 399–413. Our copy does not say that uncharacterized helices in residues 150–340 pack with it to form a tertiary fold. (LLM, conf=0.84)
hedgedconditional- 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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This is presumably due to displacement of endogenous PU.1 from an isolated Ets site in the J chain promoter”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Fused dimers as a general tool for analysis of combinatorial control of transcription in vivo
What the sources say
- Supportedcites Shin and Koshland, 1993 source
In “A PU.1 dominant negative mutant blocks PU.1 regulation of the J-chain gene promoter” (Fig. 10; page not provided), the paper reports that the N133 mutant suppressed J-chain promoter activity by competitively binding its single PU.1 site. It interprets this as preventing endogenous PU.1 from binding the JB element, supporting the proposed displacement mechanism. (LLM, conf=0.94)
hedgedconditional- 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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This is consistent with increased expression of Pip in plasma cell lines such as J558L”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
What the sources say
- Supportedcites Brass et al., 1996 source
The “Pip is NF-EM5” section reports Western blot detection of Pip in B-cell lines, including the plasmacyte line J558L, with expression increasing in later-stage cells (Fig. 1B). This supports the claim of increased Pip expression in a plasma-cell line such as J558L. (LLM, conf=0.93)
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.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Each enhancer contains an essential composite site (λB) bound by PU.1 and Pip”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
What the sources say
- Could not verifycites Hagman et al., 1990 sourceExperimental — accuracy not yet measured
The Abstract identifies two lambda enhancers, and “Cloning of a second enhancer and comparison with” discusses conserved sequence motifs. Neither passage identifies an essential λB composite site or reports binding by PU.1 and Pip; searches for those terms found no supporting passage in our copy. (LLM, conf=0.76)
- Not matchedcites Rudin and Storb 1992
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Eisenbeis et al., 1993 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
- It may state two separate claims as one. 42
- Probably not a substantial claim. 24
Every source the paper cites for this claim was checked and supports it.
In the paper
“Therefore, this domain contains structural determinants important for both PU.1 interaction and autoinhibition (Brass et al., 1996).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Introduction
What the sources say
- Supportedcites Brass et al., 1996 source
The paper’s “Structural basis for PU.1-dependent DNA-binding of Pip” section states that Pip amino acids 138–450 contain structural determinants for both autoinhibition of DNA binding and specific association with PU.1, and identifies this region as a regulatory domain. This directly supports the attributed claim. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Pip deletion mutants which retained the ability to form a ternary complex with PU.1 (1-439 and 1-419; Brass et al., 1996; data not shown) stimulated transcription comparable with full-length Pip.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
What the sources say
- Partly supportedcites Brass et al., 1996 sourceExperimental — accuracy not yet measured
In the section on Pip amino acids 410–439 (page not supplied), Brass et al. report that deleting Pip to residue 439 did not affect ternary complex formation with PU.1. Our copy does not report the 1–419 mutant or show that these two mutants stimulated transcription comparably to full-length Pip; the citing sentence labels the transcription result “data not shown.” (LLM, conf=0.86)
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.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“This linker was chosen because it flexibly connects the POU homeo-and POUspecific domains (Herr and Cleary, 1995), and appears unstructured in the Oct-1-DNA co-crystal structure (Klemm et al., 1994).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering a PU.1-Pip chimeric repressor
What the sources say
- Supportedcites Herr and Cleary, 1995 source
Herr and Cleary is cited for the linker’s flexible connection between the POU-specific and POU homeo domains. The POU domain and POU-domain linker sections explicitly describe that connection and its flexibility. The co-crystal observation is separately attributed to Klemm et al. in the citing sentence, so it is not required of this citation. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Klemm et al., 1994 source
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“As shown previously, full-length Pip cannot bind to DNA in the absence of PU.1; however, a C-terminal deletion mutant, Pip 1-410, can bind DNA independently (Figure 2A, compare lanes 2 and 3; Brass et al.,1996).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
What the sources say
- Partly supportedcites Brass et al., 1996 sourceExperimental — accuracy not yet measured
The deletion-analysis section reports that full-length Pip did not bind DNA independently in its gel-shift assay, while Pip 1–410 did. But the ‘Pip functions as a dichotomous regulator’ section says full-length Pip could bind DNA without PU.1 in cell extracts under different conditions, so the unqualified ‘cannot’ overstates the result. (LLM, conf=0.86)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“J558L B cells also express the J chain gene, the transcription of which has been suggested to be regulated by PU.1 binding to the J chain promoter”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > The PipPU chimeric repressor blocks endogenous IgL λ gene expression when stably expressed in B cells
What the sources say
- Partly supportedcites Shin and Koshland, 1993 sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that PU.1 binds a regulatory element in the J-chain promoter and activates J-chain transcription. The paper identifies S194 as a J-chain-expressing cell line, but the passages found do not establish that J558L cells express the gene; the cell-line-specific part of the claim is unsupported. (LLM, conf=0.84)
hedgedconditional- 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“we identified a predicted α-helix within Pip's C-terminus (amino acids 395-413) that is critical for both formation of a ternary complex and autoinhibition of DNA binding”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
What the sources say
- Partly supportedcites Brass et al., 1996 sourceExperimental — accuracy not yet measured
The Structural basis section postulates that a putative α-helical region may play a key role in ternary complex formation and autoinhibition; the Model section identifies that region as amino acids 399–413, not 395–413. The paper’s deletion results establish the importance of a broader segment, amino acids 410–439, but do not establish that the predicted helix itself is critical. (LLM, conf=0.88)
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.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Probes B1 and C1 differ in their flanking sequences”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering a PU.1-Pip chimeric repressor
What the sources say
- Could not verifycites Brass et al., 1996 sourceExperimental — accuracy not yet measured
The Gel mobility shift assays section describes a murine κB-site probe, and the Pip is NF-EM5 section describes complexes formed on that probe, but neither identifies probes B1 and C1 or compares their flanking sequences. Searches for “B1 and C1,” “C1 probe,” and “flanking sequences” found no passage addressing the claimed difference. (LLM, conf=0.75)
- Not matchedcites Himmelman et al., 1997
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.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“IRF-3 possesses a C-terminal autoinhibitory region.Regulated phosphorylation of this region upon viral infection stimulates DNA binding”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
What the sources say
- Partly supportedcites Lin et al., 1998 sourceExperimental — accuracy not yet measured
The Discussion proposes a C-terminal autoinhibitory domain and a model in which virus-induced phosphorylation relieves autoinhibition and leads to DNA binding; the Abstract also reports stimulated DNA binding. The claim states the proposed domain as established and implies that the autoinhibitory domain itself is phosphorylated. The Discussion places that domain at amino acids 407–427, but the phosphorylation sites at 396–405. (LLM, conf=0.84)
- Partly supportedcites Yoneyama et al., 1998 sourceExperimental — accuracy not yet measured
The Discussion reports that viral stimulation induces IRF-3 phosphorylation and sequence-specific DNA-binding activity; the Functional domains of IRF-3 section implicates C-terminal serines 385 and 386 in the virus-induced response. Our copy does not identify a C-terminal autoinhibitory region, and the Discussion says the order of phosphorylation and DNA-binding activation could not be determined. (LLM, conf=0.85)
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. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A recent study using protein-protein interaction assays suggests that PU.1 and Pip can interact in the absence of template DNA”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
What the sources say
- Supportedcites Perkel et al., 1998 source
The section “Interaction of GST-Pip and PU.1 in solution requires the PU.1 ETS domain” reports a protein-interaction assay in which PU.1 bound GST-Pip without DNA. It explicitly concludes that PU.1 and Pip can physically interact in solution. (LLM, conf=0.95)
hedgedcorrelational- 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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“recent work has shown that PU.1 nucleates a multi-transcription factor complex on the E κ3Ј”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
What the sources say
- Supportedcites Pongubala and Atchison, 1997 source
The paper states that PU.1 participates with other transcription factors in forming a higher-order complex on the immunoglobulin κ 3′ enhancer. The Discussion describes PU.1 as important to the complex’s formation and calls the mechanism nucleation of enhancer-binding proteins. The supplied passages have section labels but no page numbers. (LLM, conf=0.92)
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.
Probably not a substantial claim.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The PU.1-and Pip-binding sites have been underlined based on methylation interference analysis of the λB site(Eisenbeis et al., 1995).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
What the sources say
- Supportedcites Eisenbeis et al., 1995 source
The methylation-interference results (Fig. 2C; page unavailable in our copy) delimit the Pip-binding site adjacent to the previously determined PU.1-binding site. The Figure 2 caption says the paper compares its Pip results with methylation-interference results for PU.1, supporting the cited basis for marking both sites. (LLM, conf=0.90)
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.
- Supported
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
“Alanine substitution of amino acids 401-404 and 405-408 resulted in 9-and 15-fold increases in binding above background, respectively.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
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.
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
“Further deletion into the region encompassing the putative α-helix (1-410) severely reduced ternary complex formation and abolished synergistic activation of transcription.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
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.
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
“This mutant protein, PipAS397, is defective in its interaction with PU.1, but is autoinhibited.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
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.
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 Pip mutant (Pipmut) exhibited reduced affinity for the composite sites, and therefore its binding properties resembled those of PU.1”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering a PU.1-Pip chimeric repressor
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.
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 estimated half-life for the PipPU-DNA complex (60 min) was considerably longer than that for PU.1 (6 min) or the PU.1 DBD (8 min).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering a PU.1-Pip chimeric repressor
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.
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 significantly longer half-life of the Pipmut-DNA complex (60 min) as compared with that of the PUmut-DNA complex (6 min)”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering a PU.1-Pip chimeric repressor
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.
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
“transcriptional repression by PipPU was specific, since it did not inhibit the activity of a reporter construct containing a Vκ promoter and the intron κ enhancer”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Wild-type, Pipmut and PUmut chimeras repress λ enhancer function in transient assays
plain- Asserted: passes — The authors put it forward as true.
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“Enhancer activity was strongly inhibited by expression of the PipPU, Pipmut and PUmut, but not by the DM fused dimer”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Wild-type, Pipmut and PUmut chimeras repress λ enhancer function in transient assays
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In the paper
“The mutant protein, PipAS397, is defective in its interaction with PU.1, but is autoinhibited.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
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“resulted in the Pipmut protein, which bound DNA with similar specificity to PU.1, but with a longer half-life.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
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“the PUmut protein, which contains mutations within the PU.1 DBD, independently bound DNA with high affinity and thus acted quite differently from Pip.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
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“Pip, ICSBP and p48 possess considerably lower DNA affinity, relying on partners to form high affinity complexes.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Two IRF subgroups that are structurally and biochemically distinguishable
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“The PipPU chimera bound the λB site less well than the wild-type proteins; however, on a composite element containing a lower affinity PU.1 site, the chimera and PU.1-Pip bound equivalently.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
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In the paper
“Our strategy produced a chimera, PipPU, which preferred a composite site to a PU.1 site by a factor of 3 (λB) or 8 (CD20), correlating with the affinity of wild-type PU.1 for these sites.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
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In the paper
“Pip contains two major structural domains, a DNA-binding domain and a regulatory domain, separated by a linker.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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In the paper
“all three PipPU chimeras (PipPU, Pipmut and PUmut) repressed transcription of a λ enhancercontaining reporter in transient assays, with PipPU being somewhat more effective than the mutant chimeras.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
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In the paper
“Fusing the DBDs of Pip and PU.1 generates a chimeric protein which preferentially binds composite elements with increased stability.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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In the paper
“However, the role of PU.1-Pip complexes in regulating the expression of endogenous IgL genes remains to be elucidated.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Introduction
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“In eukaryotes, gene expression appears to be regulated by the assembly of distinct combinations of transcription factors at promoters and enhancers.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Introduction
What the sources say
- Not checked — no full text of the sourcecites Carey, 1998 source
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In the paper
“Mutation of E406 to proline also generated a protein which bound DNA independently (32-fold above background), suggesting that overall helix integrity is necessary for both autoinhibition and ternary complex formation (Figure 2A, compare lanes 2 and 12).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
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In the paper
“Therefore, the DBDs of IRF-1 and Pip have structurally diverged, such that Pip binds cooperatively with PU.1, while IRF-1 displaces PU.1 from the composite element.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > PU.1 and the DNA-binding domain of IRF-1 compete for binding to λB DNA
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In the paper
“Thus, the α-helical region in Pip's C-terminus is important for both interaction with PU.1 in vitro and transcriptional synergy in vivo.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
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In the paper
“Previous work has shown that the E λ2-4 construct (OPC 20) is preferentially active in B cells, and mutations in either the PU.1-or Pip-binding site within this construct abolish enhancer function”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Wild-type, Pipmut and PUmut chimeras repress λ enhancer function in transient assays
What the sources say
- Not checked — no full text of the sourcecites Eisenbeis et al., 1993 source
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In the paper
“Therefore, in transient assays, both the wild-type (PipPU) and mutant chimeras (Pipmut and PUmut) effectively blocked enhancer function, presumably by displacement of endogenous PU.1-Pip complexes.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Wild-type, Pipmut and PUmut chimeras repress λ enhancer function in transient assays
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In the paper
“Each of the chimeric proteins was expressed comparably with endogenous Pip and their expression did not alter wild-type Pip levels”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > The PipPU chimeric repressor blocks endogenous IgL λ gene expression when stably expressed in B cells
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In the paper
“β-actin transcripts were used both as a specificity control and for normalization.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > The PipPU chimeric repressor blocks endogenous IgL λ gene expression when stably expressed in B cells
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In the paper
“An interaction analogous to the one between PU.1 and Pip, involving the pKID domain of the CREB transcription factor and the KIX domain of the co-activator CBP, is mediated by a phosphoserine residue located within pKID”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
What the sources say
- Not checked — no full text of the sourcecites Parker et al., 1996 source
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In the paper
“A Pip deletion mutant, Pip 1-410, which does not form a ternary complex with PU.1 fails to activate transcription synergistically with PU.1.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
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In the paper
“a single hydrogen bond between this phosphoserine and a tyrosine residue within CBP is critical for complexation”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
What the sources say
- Not checked — no full text of the sourcecites Radhakrishnan et al., 1997 source
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In the paper
“Protein-protein contacts also occur between Pip's DBD and PU.1's DBD and may contribute additional specificity and stability to the ternary complex.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
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In the paper
“a binding partner, such as PU.1 or STATs, may provide these lost contacts to Pip or p48 in trans, via protein-protein interactions.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Two IRF subgroups that are structurally and biochemically distinguishable
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In the paper
“we propose that PU.1-Pip ternary complex assembly is regulated by two template-directed proteinprotein contacts, one between PU.1's PEST region and Pip's regulatory domain, and the second depending on association of PU.1's DBD with that of Pip.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
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In the paper
“The ICSBP DBD strongly repressed both interferon (IFN)-stimulated gene expression and the anti-proliferative effects of IFN, while the full-length protein had little effect on these activities.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
What the sources say
- Not checked — no full text of the sourcecites Thornton et al., 1996 source
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In the paper
“In the NFAT-AP-1-DNA complex, the Rel homology region of NFAT and the bZip domain of AP-1 make extensive contacts with one another that are both necessary and sufficient for complex formation on DNA”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
What the sources say
- Not checked — no full text of the sourcecites Chen et al., 1998 source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This association is dependent on multiple residues within Pip's interaction helix, including an electrostatic interaction between Pip's Lys399 and PU.1's pSer148.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Cooperative binding by PU.1 and Pip is regulated by multiple interdependent DNA-protein and protein-protein interactions
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In the paper
“Previous studies have either created chimeric transcription factors which recognize synthetic regulatory elements by fusing domains from biologically unrelated proteins, or used phage display technology to create a zinc finger protein which recognizes a DNA site generated by a chromosomal translocation”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
What the sources say
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“this approach not only serves to test the proposed functions of interacting activators in vivo, but should also enable the identification of novel genes specifically regulated by such activator complexes.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Fused dimers as a general tool for analysis of combinatorial control of transcription in vivo
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In the paper
“Pip-deficient animals develop normal numbers of B cells (including λ-expressors) which cannot undergo activation”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
What the sources say
- Not checked — no full text of the sourcecites Mittrucker et al., 1997 source
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In the paper
“The structures of all constructs were confirmed by dideoxy sequencing.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Plasmids
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In the paper
“PU.1 and the chimeric proteins are present in equimolar amounts.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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In the paper
“Each determination represents the average of at least three independent experiments.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Gel mobility shift assays
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In the paper
“The proteins were Ͼ80% pure as judged by densitometric analysis of Coomassie Blue-stained 12.5% SDS-PAGE gels.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Protein purification
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In the paper
“Fold-activation (solid bars) indicates CAT activity normalized to the control expression vector and is the average of two independent experiments.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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In the paper
“This may be attributable to the higher ratio of target DNA to non-specific DNA as well as increased levels of protein expression in a transient assay.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
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In the paper
“These data are representative of three independent experiments each using different RNA preparations.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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In the paper
“Solid bars indicate average CAT activity (percentage chloramphenicol acetylation) of two independent transfections.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“This contact is mediated by multiple residues in Pip's interaction helix, including an electrostatic interaction between K399 of Pip and PU.1's pSer148 (P-S148).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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In the paper
“Equimolar amounts of Pip or PipK399A, and PU.1 or PU.1S148A were used in the binding reactions.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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, Pip is dispensable for IgL λ transcription during B cell development but may be required for the enhanced expression of this locus during B cell activation and terminal differentiation.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Engineering PU.1-Pip chimeric repressors
hedgedconditional- 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.
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
“Equimolar amounts of the Pip proteins were used based on PhosphorImager analysis of SDS-PAGE gels.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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.
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
“All Pip proteins are present in equimolar amounts.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Northern blot analysis
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.
The paper relies on this without support.
PU.1 and Pip act as mutually dependent transcriptional activators in vivo.
“As noted, PU.1 and Pip function as mutually dependent transcriptional activators in vivo.”
The paper relies on this without support.
The λB probe's high-affinity PU.1 site (AAGGAA) could mask some of the DNA-binding gain provided by fusing the Pip DBD.
“The λB probe contains a high affinity PU.1-binding site (AAGGAA), which might mask some of the gain in DNA binding provided by the fusion of the Pip DBD.”
The paper relies on this without support.
The CD20 composite element contains a lower-affinity PU.1-binding site (AAAGAA).
“the composite element from the CD20 promoter, which contains a lower affinity PU.1-binding site (AAAGAA”
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 cited source says what the claim attributes to it.
In the citing paper
“Similar protein-protein interaction between PU.1 and PIP has been detected in the Ig λ light chain enhancer and the CD20 promoter (27-29”
From AKT Induces Transcriptional Activity of PU.1 through Phosphorylation-mediated Modifications within Its Transactivation Domain (2001) · cites this paper as [28]
In the citing paper
“A model was proposed for PU.1/Pip ternary complex. In this two-step recruitment mechanism, PU.1/Pip interaction is DNA template-directed and involves two distinct protein–protein interaction surfaces: (i) the ETS (PU.1) and IRF (Pip) DNA binding domains and (ii) the phosphorylated PEST domain of PU.1 and a putative α helix in Pip [118, 119] (Fig. 9).”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [119]
In the citing paper
“More dramatically, however, the phosphorylated PEST sequence of SPI1 interacts with an autoinhibitory region of IRF4 to enhance DNA binding by almost three orders of magnitude (154).”
From Genomic and biochemical insights into the specificity of ETS transcription factors (2011) · cites this paper as [154]
In the citing paper
“The low affinity of the winged helix-turn-helix DNA-binding domain of IRF4 for the λB enhancer is increased 20–40-fold by the presence of SPI1 at this site (154, 155).”
From Genomic and biochemical insights into the specificity of ETS transcription factors (2011) · cites this paper as [154]
In the citing paper
“the PU.1-ICSBP interaction is dependent on the IAD domain in the C-terminal region, although the DBD is also required for this interaction (5, 38).”
From Gamma Interferon Triggers Interaction between ICSBP (IRF-8) and TEL, Recruiting the Histone Deacetylase HDAC3 to the Interferon-Responsive Element (2002) · cites this paper as [5]
In the citing paper
“ICSBP has been known to interact with PU.1, a hematopoietic-cellspecific member of the Ets family (4, 5, 38).”
From Gamma Interferon Triggers Interaction between ICSBP (IRF-8) and TEL, Recruiting the Histone Deacetylase HDAC3 to the Interferon-Responsive Element (2002) · cites this paper as [5]
In the citing paper
“PU.1 requires the PEST domain, which is N-terminal to the Ets domain, for interacting with ICSBP (5).”
From Gamma Interferon Triggers Interaction between ICSBP (IRF-8) and TEL, Recruiting the Histone Deacetylase HDAC3 to the Interferon-Responsive Element (2002) · cites this paper as [5]
In the citing paper
“It also associates with PU.1 and stimulates activity of the Ets/IRF composite element (EICE), which also contains IRS and is present in the immunoglobulin (Ig) k and l , gp91 phox , scavenger receptor, toll-like receptor-4 (TLR-4), and interleukin (IL)-1 b genes. (5,23,26-30)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [26]
In the citing paper
“Notably, Irf8 peaks were enriched for EICE motifs, which are co-bound by PU.126.”
From Single-cell analysis of mixed-lineage states leading to a binary cell fate choice (2016) · cites this paper as [26]
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
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
“The λB composite element (AAAGGAAGTGAAACCA) contains a PU.1-binding site at its 5Ј end separated by 2 bp from the Pip-binding site.”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Two IRF subgroups that are structurally and biochemically distinguishable
“Comparison of the IRF recognition site (GAGAAGTGAAAGT, IRF-1 core in bold) with the λB EICE (AAGGAGTGAAACC, PU.1 core emboldened)”
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
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
“Next, we attempted to disrupt the folding of the interaction helix by substituting a proline for glutamine at position 406 (PipE406P).”
§ Assembly requirements of PU.1-Pip (IRF-4) activator complexes: inhibiting function in vivo using fused dimers > Results
“Importantly, mutation of this Glu406 to an alanine had no effect on ternary complex formation, indicating that the nature of the side chain was not critical (data not shown).”
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“1 fusion functions as a sequence-specific transcriptional repressor (Brass et al., 1999).”
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Transcriptional Regulation of Germinal Center B and Plasma Cell Fates by Dynamical Control of IRF4
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InfluentialSelf-citationSingle-cell analysis of mixed-lineage states leading to a binary cell fate choice
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Self-citationPathogenesis of Human B Cell Lymphomas
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“IRF4 constructs have been published previously (19, 20).”
BackgroundSelf-citationHematopoietic cytokines, transcription factors and lineage commitment
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“The interferon consensus sequence binding protein (ICSBP/IRF-8), a putative transcriptional partner of PU.1 (Brass et al., 1999), was recently found to be essential for monocytic development while inhibiting the production of neutrophils from GMCSF-dependent ICSBP7/7 cell line Tot2 and granulocytic…”
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ICSBP Directs Bipotential Myeloid Progenitor Cells to Differentiate into Mature Macrophages
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“PU.1 can bind to Ets binding sites on its own, but PU.1 also cooperates with IRF4 or IRF8 at Ets-IRF composite response elements called EICEs (Brass et al., 1999).”
IRF-4,8 orchestrate the pre-B-to-B transition in lymphocyte developmentPreprint
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“IRFs may also bind in complex with SPI1, another hematopoietic factor, forming a longer TFBS (Brass et al. 1999).”
BackgroundInfluentialThe genetic network controlling plasma cell differentiation
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BackgroundIRF4: Immunity. Malignancy! Therapy?
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“(4,24,25) It 26–30) Interactions with IRF-1/2 and PU.1 significantly enhance DNA-binding activity of ICSBP and are mediated through the IAD.”
MUM1/IRF4 expression as a frequent event in mature lymphoid malignancies
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Transcription Factors in Lymphocyte Development— T and B Cells Get Together
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Self-citationDirect Inhibition of IRF-Dependent Transcriptional Regulatory Mechanisms Associated With Disease
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“1-IRF4 dimer can potently represses the expression of the immunoglobulin lambda gene (the small polypeptide subunit of any antibody), and thus is of critical importance in the regulation of B cell gene expression (108).”
BackgroundCrystal structure of PU. 1/IRF-4/DNA ternary complex
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“1 (SPI-1) protein at the k and j enhancer segments of immunoglobulin (Ig) genes, where it is essential for the expression of a productively rearranged immunoglobulin gene (19).”
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“For instance, IRF9 (ISGF3g) recruits tyrosine-phosphorylated STAT1 and/or STAT2 proteins (3, 41, 47) while IRF4 (Pip) and IRF8 (ICSBP) recruit the Ets protein PU.1 ( 6 , 7). This domain, which has been referred to as the IRF association domain (IAD), is capable of mediating dimer formation among IRF partners as well a…”
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BackgroundMethodThe IgH Locus 3′ Regulatory Region
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“Among interferon-induced factors, IRF4 /Pip synergistically interacts with PU.1 and E47 but this effect is inhibited by Bcl6 in GC and Blimp1 in plasma cells (Brass et al., 1999; Gupta et al., 2001; Nagulapalli and Atchison, 1998).”
BackgroundMonocyte differentiation and macrophage polarization
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“Among the pro-inflammatory genes induced by IRF-8 are IL-12p40, IL-12p35, IFN-β, and iNOS, that are characteristic for the M1 macrophage phenotype[55].”
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“87 nM, which is similar to a previously determined Kd for its binding to this site (34).”
BackgroundEssential role of interferon regulatory factor 4 (IRF4) in immune cell development
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“factors), an auto-inhibitory domain, and a nuclear-localization signal (Brass et al. 1999) (Fig.”
BackgroundWhen Ets transcription factors meet their partners
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Immune cell-specific amplification of interferon signaling by the IRF-4/8-PU. 1 complex
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“39,40 Cocrystallization of the PU.1 Ets domain and IRF-4 DNA-binding domain bound to the EICE DNA revealed a 3D structure of the complex and important contact residues.”
Fate Decisions Regulating Bone Marrow and Peripheral B Lymphocyte Development
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Interferon regulatory factor 4 and 8 in B-cell development
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“1 or Spi-B and bind to the Ets-IRF composite element (EICE; GGAAnnGAAA) located in immunoglobulin (Ig) light chain κ 3’ (Ek3’) and λ gene enhancer regions [2-4].”
BackgroundMarecki, S., Riendeau, C. J., Liang, M. D., & Fenton, M. J. (2001) · The Journal of Immunology · doi:10.4049/jimmunol.166.11.6829 · Cited by 111
“1/IRF-4 synergy, reminiscent of the activity of K399A IRF-4 in macrophages, a finding consistent with previous studies (27).”
InfluentialIRF4 regulates IL-17A promoter activity and controls RORγt-dependent Th17 colitis in vivo
Mudter, J., Yu, J., Zufferey, C., Brüstle, A., Wirtz, S. J., Weigmann, B., Hoffman, A. W., Schenk, M., Galle, P. R., Lehr, H. A., et al. (2011) · Inflammatory Bowel Diseases · doi:10.1002/ibd.21476 · Cited by 108
“1.(15) IRF4 is expressed in B cells, mature T cells, dendritic cells, and macrophages, and its expression is up-regulated by IgM or TCR crosslinking as well as costimulation in lymphocytes.”
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Posttranslational Regulation of IRF-4 Activity by the Immunophilin FKBP52
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IFN Regulatory Factor 4 and 8 Promote Ig Light Chain κ Locus Activation in Pre-B Cell Development
Ma, S., Turetsky, A., Trinh, L. X., & Lu, R. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.11.7898 · Cited by 95
NF-IL6 (C/EBPβ) Vigorously Activates il1b Gene Expression via a Spi-1 (PU.1) Protein-Protein Tether
Yang, Z., Wara-aswapati, N., Chen, C., Tsukada, J., & Auron, P. E. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.m000145200 · Cited by 92
Martinvalet, D. (2018) · Cell Death and Disease · doi:10.1038/s41419-017-0237-7 · Cited by 94
Reactive Oxygen Species: Do They Play a Role in Adaptive Immunity?
Bassoy, E. Y., Walch, M., & Martinvalet, D. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.755856 · Cited by 93
Transcriptional determinants of tolerogenic and immunogenic states during dendritic cell maturation
Lugt, B. V., Riddell, J., Khan, A. A., Hackney, J. A., Lesch, J., DeVoss, J., Weirauch, M. T., Singh, H., & Mellman, I. (2017) · The Journal of Cell Biology · doi:10.1083/jcb.201512012 · Cited by 85
Self-citationMarecki, S., Atchison, M. L., & Fenton, M. J. (1999) · The Journal of Immunology · doi:10.4049/jimmunol.163.5.2713 · Cited by 87
Guria, S., Hoory, A., Das, S., Chattopadhyay, D., & Mukherjee, S. (2023) · Bioscience Reports · doi:10.1042/bsr20220200 · Cited by 105
Banerjee, S., Lu, J. L., Cai, Q., Saha, A., Jha, H. C., Dzeng, R. K., & Robertson, E. S. (2013) · PLoS Pathogens · doi:10.1371/journal.ppat.1003314 · Cited by 81
“So, it was possible that IRF4 interacts with EBNA3C through a Spi-1 or Spi-B motif.”
BackgroundInfluentialTargeting IRF4 in autoimmune diseases
Xu, W., Pan, H., Ye, D., & Xu, Y. (2012) · Autoimmunity Reviews · doi:10.1016/j.autrev.2012.08.011 · Cited by 82
“IRF4 protein comprises a single polypeptide chain [9] that could be roughly split into three parts: a functional regulatory domain containing two transactivation domains (TAD) and regions required for ternary complex formation and auto-suppression [10], a highly conserved N-terminal DNA-binding domain (DBD), which is…”
BackgroundIRF4 in multiple myeloma—Biology, disease and therapeutic target
Agnarelli, A., Chevassut, T. J. T., & Mancini, E. J. (2018) · Leukemia Research · doi:10.1016/j.leukres.2018.07.025 · Cited by 75
IRF4 and its regulators: evolving insights into the pathogenesis of inflammatory arthritis?
Biswas, P. S., Bhagat, G., & Pernis, A. B. (2009) · Immunological Reviews · doi:10.1111/j.0105-2896.2009.00864.x · Cited by 84
Little, H., Rorick, N. K., Su, L.-I., Baldock, C., Malhotra, S., Jowitt, T., Gakhar, L., Ramaswamy, S., Schutte, B. C., Dixon, M. J., et al. (2008) · Human Molecular Genetics · doi:10.1093/hmg/ddn381 · Cited by 80
Gupta, P., Gurudutta, G. U., Saluja, D., & Tripathi, R. P. (2009) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2009.00757.x · Cited by 74
“Specifically, the first step involves an interaction between the DNA binding domains of PU.1 and Pip.”
BackgroundInfluentialPU.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
“1 and IRF-4 DBDs, connected by a flexible linker, inhibited Ig λ light chain enhancer expression in B cells, implying in vivo binding of this element (110).”
BackgroundIRF4 haploinsufficiency in a family with Whipple’s disease
Guérin, A., Kerner, G., Marr, N., Markle, J., Fenollar, F., Wong, N., Boughorbel, S., Avery, D. T., Ma, C. S., Bougarn, S., et al. (2018) · eLife · doi:10.7554/elife.32340 · Cited by 75
PU.1 cooperates with IRF4 and IRF8 to suppress pre-B-cell leukemia
Pang, S. H. M., Minnich, M., Gangatirkar, P., Zheng, Z., Ebert, A., Song, G., Dickins, R. A., Corcoran, L. M., Mullighan, C. G., Busslinger, M., et al. (2016) · Leukemia · doi:10.1038/leu.2016.27 · Cited by 69
Kuwata, T., Gongora, C., Kanno, Y., Sakaguchi, K., Tamura, T., Kanno, T., Basrur, V., Martinez, R., Appella, E., Golub, T., et al. (2002) · Molecular and Cellular Biology · doi:10.1128/mcb.22.21.7439-7448.2002 · Cited by 69
Care, M. A., Cocco, M., Laye, J. P., Barnes, N., Huang, Y., Wang, M., Barrans, S., Du, M., Jack, A., Westhead, D. R., et al. (2014) · Nucleic Acids Research · doi:10.1093/nar/gku451 · Cited by 65
Review: 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
“(93) Also, Oritz et al. (94) identified aa 300–314 and 325–335 as the locations of two predicted a -helices that are also involved in PU.1/IRF-4 protein-protein interaction.”
IRF4 and IRF8: governing the virtues of B lymphocytes
Shukla, V., & Lu, R. (2014) · Frontiers in Biology · doi:10.1007/s11515-014-1318-y · Cited by 70
“Early studies identi fi ed IRF4 and IRF8 as transcription factors that bind the 3 ′ κ enhancer and λ enhancer to regulate the rearrangement and expression of immunoglobulin light chain at the pre-B cell stage (Brass et al., 1996; Brass et al., 1999; Ma et al., 2006).”
Carbone, A., Gloghini, A., Cozzi, M. R., Capello, D., Steffan, A., Monini, P., Marco, L. D., & Gaïdano, G. (2000) · British Journal of Haematology · doi:10.1046/j.1365-2141.2000.02329.x · Cited by 67
Gosselin, D., & Glass, C. K. (2014) · Immunological Reviews · doi:10.1111/imr.12213 · Cited by 66
“1 protein may also modulate its activity in certain conditions (100).”
BackgroundIRF8: Mechanism of Action and Health Implications
Moorman, H. R., Reategui-Almonacid, Y., Poschel, D. B., & Liu, K. (2022) · Cells · doi:10.3390/cells11172630 · Cited by 63
Review: The Role of IRF-4 in B and T Cell Activation and Differentiation
Pernis, A. B. (2002) · Journal of Interferon & Cytokine Research · doi:10.1089/107999002753452728 · Cited by 63
“(41) Interestingly, an additional IRF-4 binding site within the k 3 9 enhancer has also been identified.”
Shin, D., Lee, C., & Morse, H. C. (2011) · PLoS ONE · doi:10.1371/journal.pone.0027384 · Cited by 59
“1 and IRF4 to regulate gene expression through recognition of ISRE and EICE sequence elements [1,49].”
BackgroundO’Reilly, D., Quinn, C. M., El‐Shanawany, T., Gordon, S., & Greaves, D. R. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m212150200 · Cited by 56
Unlu, S., Kumar, A., Waterman, W. R., Tsukada, J., Wang, K. Z. Q., Galson, D. L., & Auron, P. E. (2007) · Molecular Immunology · doi:10.1016/j.molimm.2007.02.016 · Cited by 57
“This argues that a complex containing, in-part, a Spi-1•IRF association similar to that observed for the IgλL and 3′IgκL light-chain enhancers (Brass et al., 1996;Brass et al., 1999;Escalante et al., 2002;Perkel and Atchison, 1998) is important for activity.”
BackgroundInfluentialBertolino, E., & Singh, H. (2002) · Molecular Cell · doi:10.1016/s1097-2765(02)00597-x · Cited by 54
Self-citationRieske, P., & Pongubala, J. R. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m007482200 · Cited by 54
Csumita, M., Csermely, A., Horváth, A., Nagy, G., Monori, F., Göczi, L., Orbea, H. A., Reith, W., & Széles, L. (2019) · Nucleic Acids Research · doi:10.1093/nar/gkz1112 · Cited by 48
“These results do not imply necessarily that IRF3dimers and ISGF3 (STAT1/STAT2/IRF9) bind EICE motif with a high frequency.”
MethodInfluentialTranscriptional Control of Mature B Cell Fates
Wang, H., Morse, H. C., & Bolland, S. M. (2020) · Trends in Immunology · doi:10.1016/j.it.2020.04.011 · Cited by 50
Arguello, M., Sgarbanti, M., Hernandez, E., Mamane, Y., Sharma, S., Servant, M. J., Lin, R., & Hiscott, J. B. (2003) · Oncogene · doi:10.1038/sj.onc.1206270 · Cited by 52
“This site is coordinately regulated by the transcription factors PU.1 and IRF-4, which form a ternary complex and synergistically activate transcription (Brass et al., 1996, 1999).”
BackgroundAnderson, M. K., Sun, X. H., Miracle, A. L., Litman, G. W., & Rothenberg, E. V. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.98.2.553 · Cited by 53
Verger, A., Buisine, E., Carrère‐Kremer, S., Wintjens, R. T., Flourens, A., Coll, J., Stéhelin, D., & Duterque‐Coquillaud, M. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m010208200 · Cited by 50
Interferon Regulatory Factor Signalings in Cardiometabolic Diseases
Zhang, X., Zhang, P., & Li, H. (2015) · Hypertension · doi:10.1161/hypertensionaha.115.04898 · Cited by 51
“1 and SPI-1 or with heterodimers of JUN and basic leucine zipper transcription factor, activating transcription factor-like.(13,14) For IRF5, a homodimer or a heterodimer with IRF3 or IRF7 could be formed after activation.”
BackgroundAnalysis of Gene Expression and Ig Transcription in PU.1/Spi-B-Deficient Progenitor B Cell Lines
Schweitzer, B. L., & DeKoter, R. P. (2004) · The Journal of Immunology · doi:10.4049/jimmunol.172.1.144 · Cited by 51
“1-IFN regulatory factor (IRF)-4 forced dimer lacking activation domains has been shown to silence Ig transcription in a B cell line (56).”
BackgroundPU.1 and ICSBP control constitutive and IFN-γ-regulatedTlr9gene expression in mouse macrophages
Schroder, K., Lichtinger, M., Irvine, K. M., Brion, K., Trieu, A., Ross, I. L., Ravasi, T., Stacey, K. J., Rehli, M., Hume, D. A., et al. (2007) · Journal of Leukocyte Biology · doi:10.1189/jlb.0107036 · Cited by 51
“1 complex to DNA by EMSA analysis using nuclear extracts from untransfected cells; instead, many used in vitro-translated protein [65–68] or nuclear extracts from transfected cells [69].”
MethodMatsumura, I., Kawasaki, A., Tanaka, H., Sonoyama, J., Ezoe, S., Minegishi, N., Nakajima, K., Yamamoto, M., & Kanakura, Y. (2000) · Blood · doi:10.1182/blood.v96.7.2440 · Cited by 53
Suzuki, Y., Yasuike, M., Kondo, H., Aoki, T., & Hırono, I. (2010) · Fish & Shellfish Immunology · doi:10.1016/j.fsi.2010.09.010 · Cited by 49
“This IAD contains RKL amino acid residues which are important to construct of the dimer or trimer with other IRFs and molecules in IRF4 and IRF8 in mammal [58].”
BackgroundBathige, S. D. N. K., Whang, I., Umasuthan, N., Lim, B.-S., Park, M.-A., Kim, E., Park, H., & Lee, J. (2012) · Fish & Shellfish Immunology · doi:10.1016/j.fsi.2012.07.017 · Cited by 48
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Transcriptional Regulation of Mouse μ Opioid Receptor Gene by PU.1
Hwang, C. K., Kim, C. S., Choi, H. S., McKercher, S. R., & Loh, H. H. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m400755200 · Cited by 46
Haro, L. D. (2002) · Nucleic Acids Research · doi:10.1093/nar/gkf390 · Cited by 45
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Carrascosa, L. C., Klein, M., Kitagawa, Y., Lückel, C., Marini, F., König, A., Guralnik, A., Raifer, H., Hagner-Benes, S., Raedler, D., et al. (2017) · Nature Communications · doi:10.1038/ncomms15366 · Cited by 41
Teng, Y., Takahashi, Y., Yamada, M., Kurosu, T., Koyama, T., Miura, O., & Miki, T. (2007) · European Journal of Cell Biology · doi:10.1016/j.ejcb.2007.05.006 · Cited by 43
“1 complex has been shown to act as a transcriptional regulator for the B-cell specific genes, such as the rearranged lambda lightchain gene (Brass et al., 1999).”
Background
Metadata
- Authors
- Brass, A. L., Zhu, A. Q., & Singh, H.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Singh, Harinder
- ORCID
- Singh, Harinder
- Venue
- The EMBO Journal
- Published
- 1999-02-15
- Volume
- 18
- Issue
- 4
- Pages
- 977-991
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC1171190
- OpenAlex
- W2121496836
- Semantic Scholar
- a3891c3b25fac116b2b2c86acc2cf094353cc3d7
- Cited by
- 204
- References
- 64
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 8 · 2023: 8 · 2022: 6 · 2021: 9 · 2020: 9 · 2019: 7 · 2018: 8 · 2017: 8 · 2016: 6 · 2015: 5 · 2014: 6 · 2013: 9 · 2012: 8
- FWCI
- 4.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- University of Toronto
- National Institutes of Health
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-07009)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Keywords
- PU.1, IRF4, Pip, ETS transcription factors, transcription factor interaction, B cell gene expression, transcriptional repression, protein-DNA contacts, protein-protein interaction surfaces
- MeSH terms
- Interferon Regulatory Factor-4, Proto-Oncogene Protein Spi-1, Amino Acid Sequence, Animals, B-Lymphocytes, DNA-Binding Proteins, Enhancer Elements, Genetic, Gene Expression Regulation, Immunoglobulin lambda-Chains, Molecular Sequence Data, Mutation, Proto-Oncogene Proteins, Recombinant Fusion Proteins, Repressor Proteins, Transcription Factors, Transfection, Tumor Cells, Cultured, Protein Engineering, Transcriptional Activation, Trans-Activators, Sequence Alignment, Dimerization, Interferon Regulatory Factors, Mice
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