The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
Pip, a lymphoid-restricted IRF, contains a regulatory domain that is important for autoinhibition and ternary complex formation with the Ets factor PU.1.
Open accessAbstract
Pip is a lymphoid-restricted IRF transcription factor that is recruited to composite elements within immunoglobulin light-chain gene enhancers through a specific interaction with the Ets factor PU.1. We have examined the transcriptional regulatory properties of Pip as well as the requirements for its interaction with PU.1 and DNA to form a ternary complex. We demonstrate that Pip is a dichotomous regulator; it specifically stimulates transcription in conjunction with PU.1, but represses alpha/beta-interferon-inducible transcription in the absence of PU.1. Thus, during B-cell activation and differentiation, Pip may function both as an activator to promote B cell-specific gene expression and as a repressor to inhibit the antiproliferative effects of alpha/beta-interferons. Mutational analysis of Pip reveals a carboxy-terminal segment that is important for autoinhibition of DNA binding and ternary complex formation. A domain of Pip containing this segment confers autoinhibition and PU.1-dependent binding activity to the DNA-binding domain of the related IRF family member, p48. On the basis of these and other data we propose a model for PU.1/Pip ternary complex formation.
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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
“A C-terminal regulatory domain within Pip itself is also required for ternary complex assembly (Brass et al., 1996).”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
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
“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.”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
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
“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).”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
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
“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”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
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
“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.”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
Experimental — accuracy not yet measured
The cited source says what the claim attributes to it.
In the citing paper
“In addition, this regulatory domain autoinhibits binding of Pip to DNA in the absence of PU.1.”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
The cited source says what the claim attributes to it.
In the citing paper
“Therefore, this domain contains structural determinants important for both PU.1 interaction and autoinhibition (Brass et al., 1996).”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
The cited source says what the claim attributes to it.
In the citing 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).”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
The cited source says what the claim attributes to it.
In the citing paper
“PU.1 and Pip represent the major components of the ternary complex formed with nuclear extract from these cells”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
The cited source says what the claim attributes to it.
In the citing paper
“This is consistent with increased expression of Pip in plasma cell lines such as J558L”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Probes B1 and C1 differ in their flanking sequences”
From Assembly requirements of PU.1–Pip (IRF‐4) activator complexes: inhibiting function in vivo using fused dimers (1999) · cites this paper as Brass et al., 1996
Experimental — accuracy not yet measuredIn the citing paper
“Pip/NF-EM5/IRF-4, a member of IRF family, is a lymphoid-restricted transcription factor that is recruited to a composite element (IRF/ETS-binding site) within Ig light chain enhancers through a specific interaction with PU.1 protein [116, 117].”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [117]
In the citing paper
“In the second step, phosphorylation of PU.1 at Ser 148 results in a conformational change in Pip (either before or after interaction with Pip) allowing cooperative DNA binding [117].”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [117]
In the citing paper
“Analogous to the PU.1-Pip interaction, the PU.1-ICSBP interaction is DNA directed and facilitated by EICE (4, 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 [4]
In the citing paper
“Although the majority of IRF family members are expressed broadly in many cell types, ICSBP and another member, Pip (IRF-4), are expressed only in the immune system (4, 12, 49).”
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 [4]
In the citing paper
“The PU.1ICSBP complex and the PU.1-Pip complex are shown to act as a stimulators of EICE-mediated transcription (4, 40).”
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 [4]
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 [4]
In the citing paper
“IRF-4 is similar to ICSBP in structure, interacts with some common partners (PU.1 and E47), and regulates an overlapping set of target promoters. (31,32,63,64)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [64]
In the citing paper
“IRF-4 is similar to ICSBP in structure, interacts with some common partners (PU.1 and E47), and regulates an overlapping set of target promoters. (31,32,63,64)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [64]
In the citing paper
“IRF-4 is similar to ICSBP in structure, interacts with some common partners (PU.1 and E47), and regulates an overlapping set of target promoters. (31,32,63,64)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [64]
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 [27]
In the citing paper
“PIP is expressed exclusively in the lymphoid lineages (27”
From AKT Induces Transcriptional Activity of PU.1 through Phosphorylation-mediated Modifications within Its Transactivation Domain (2001) · cites this paper as [27]
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Citations
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“The target sequence is called as an ETS-IRF composite element (Brass et al. 1996).”
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“4A) contains a stretch of basic amino acids and could interact with the C terminus, as has been described for other transcription factors, such as interferon response factor (IRF) family members (60).”
BackgroundCai, M., & Chen, N. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.817069 · Cited by 10
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“The interaction of IRF proteins with other transcription factors as been also described (Brass et al., 1996, 1999; Kuwata et al., 002; Perkel and Atchison, 1998).”
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BackgroundInfluential
Metadata
- Authors
- Brass, A. L., Kehrli, E., Eisenbeis, C. F., Storb, U., & Singh, H.
- Affiliations
- Howard Hughes Medical Institute (US)
- ORCID
- Singh, H
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1996-09-15
- Volume
- 10
- Issue
- 18
- Pages
- 2335-2347
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2005606581
- Cited by
- 242
- References
- 49
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 4 · 2023: 3 · 2022: 5 · 2021: 5 · 2020: 6 · 2019: 7 · 2018: 4 · 2017: 6 · 2016: 4 · 2015: 6 · 2014: 7 · 2013: 15 · 2012: 11
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- York University
- National Institutes of Health
- U.S. Public Health Service (FM07183)
- National Institute of General Medical Sciences (T32GM007281, GM-07281)
- 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 › interferon and immune responses
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- Pip, interferon regulatory factors, PU.1, ETS transcription factors, ternary complex formation, autoinhibition, B cell activation, transcriptional repression, p48, DNA-binding domain
- MeSH terms
- Interferon Regulatory Factor-8, Interferon Regulatory Factor-4, Proto-Oncogene Protein Spi-1, Animals, B-Lymphocytes, Binding Sites, Carrier Proteins, DNA-Binding Proteins, Gene Expression Regulation, Interferon-gamma, Models, Molecular, Nucleic Acid Conformation, Protein Conformation, Proto-Oncogene Proteins, Regulatory Sequences, Nucleic Acid, Repressor Proteins, Transcription Factors, Transcription, Genetic, Trans-Activators, Interferon-alpha, Interferon-Stimulated Gene Factor 3, Interferon-Stimulated Gene Factor 3, gamma Subunit, Interferon Regulatory Factors, Mice
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