The p50 subunit of NF-kappa B associates with the NF-IL6 transcription factor.

LeClair, Kenneth; Blanar, Michael A.; Sharp, Phillip A.

doi:10.1073/pnas.89.17.8145

Cited by 303 publications

(146 citation statements)

References 32 publications

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“…The cross-coupling of NF-KB with c-Jun and c-Fos has also been shown to enhance transcriptional activation through both KB and AP-1 response elements in HeLa cells (69). NF-KB also associates with members of the C/EBP transcription factor family (38,70). ATF2, c-Jun, c-Fos, and C/EBP all contain the bZIP DNA-binding and dimeriza- tion domain which mediates the physical interaction with NF-KB (17,69,70).…”

Section: Methodsmentioning

confidence: 99%

An interaction between the DNA-binding domains of RelA(p65) and Sp1 mediates human immunodeficiency virus gene activation.

Perkins¹,

Agranoff²,

Pascal³

et al. 1994

Mol. Cell. Biol.

225

157

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Induction of human immunodeficiency virus type 1 (HIV-1) gene expression in stimulated T cells has been attributed to the activation of the transcription factor NF-KB. The twice-repeated KB sites within the HIV-1 long terminal repeat are in close proximity to three binding sites for Spl. We have previously shown that a cooperative interaction of NF-KB with Spl is required for the efficient stimulation of HIV-1 transcription. In this report, we define the domains of each protein responsible for this effect. Although the transactivation domains seemed likely to mediate this interaction, we find, surprisingly, that this interaction occurs through the putative DNA-binding domains of both proteins. Spl specifically interacted with the amino-terminal region of ReIA(p65). Similarly, RelA bound directly to the zinc finger region of Spl. This interaction was specific and resulted in cooperative DNA binding to the icB and Spl sites in the HIV-1 long terminal repeat. Furthermore, the amino-terminal region of RelA did not associate with several other transcription factors, including MyoD, E12, or Koxl5, another zinc finger protein. These findings suggest that the juxtaposition of DNA-binding sites promotes a specific protein interaction between the DNA-binding regions of these transcription factors. This interaction is required for HIV transcriptional activation and may provide a mechanism to allow for selective activation of KB-regulated genes.

show abstract

Section: Methodsmentioning

confidence: 99%

An interaction between the DNA-binding domains of RelA(p65) and Sp1 mediates human immunodeficiency virus gene activation.

Perkins¹,

Agranoff²,

Pascal³

et al. 1994

Mol. Cell. Biol.

225

157

View full text Add to dashboard Cite

show abstract

“…The reporter plasmid containing the whole human GL ⑀ promoter with mutations in the C/EBP site 5Ј to the Stat6 site cannot be induced by IL-4 in human B lymphoma cells DND39 (21), indicating that C/EBP proteins are required for IL-4 inducibility of the human GL ⑀ promoter. Interestingly, physical association and functional synergism between C/EBP␤ and NF-B have also been previously demonstrated (56,57). Therefore, the proposed model for induction of mouse GL ⑀ promoter by AP-1, Stat6, and NF-B should also apply for induction of human GL ⑀ promoter, except the role of AP-1 may be substituted by C/EBP␤ in human.…”

Section: Regulation Of Ig Gl ⑀ Transcripts Differs Between Mouse and mentioning

confidence: 99%

Activation of the Mouse Ig Germline ε Promoter by IL-4 Is Dependent on AP-1 Transcription Factors

Shen

Stavnezer

2001

The Journal of Immunology

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Induction of germline (GL) ε transcripts, an essential step preceding Ig isotype switching to IgE, requires activation of transcription factors by IL-4 and a B cell activator, e.g., CD40 ligand or LPS. We demonstrate that AP-1 (Fos and Jun), induced transiently by CD40 ligand or LPS, binds a DNA element in the mouse GL ε promoter. AP-1 synergizes with Stat6 to activate both the intact GL ε promoter and a minimal heterologous promoter driven by the AP-1 and Stat6 sites of the mouse GL ε promoter. By contrast, C/EBPβ, which trans-activates the human GL ε promoter, inhibits IL-4 induction of the mouse promoter, probably by attenuating the synergistic interaction between AP-1 and Stat6. Furthermore, AP-1 does not trans-activate the human GL ε promoter. Thus, induction of GL ε transcripts in mice and humans may be regulated differently. In addition, although mouse GL ε transcripts have a half-life of ∼100 min, the RNA level continues to increase for up to 24 h, and the promoter appears to be active for at least 2 days after B cell activation. Altogether, these data suggest that induction of AP-1 activity, although transient, is required for activation of the mouse GL ε promoter by IL-4-induced Stat6.

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“…Thus, with a relatively small number of transcriptional regulators, the expression of a large number of target genes can be tightly controlled. Recent studies have suggested that interactions between C͞EBP members and CREB͞ATF (13), Fos-Jun family (14), and NF-B proteins (15,16) may occur, increasing the pool of available interacting transcription factors.…”

mentioning

confidence: 99%

CCAAT/enhancer binding protein ɛ is preferentially up-regulated during granulocytic differentiation and its functional versatility is determined by alternative use of promoters and differential splicing

Yamanaka

Kim

Radomska

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

169

157

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Hematopoietic stem cells have the ability to promote continuous self-renewal by controlled proliferation and expansive differentiation into all cells of hematopoietic lineages. Regulation of the molecular mechanisms that direct cellular proliferation and differentiation during hematopoiesis depends, partly, on the action of certain transcription factors (1-3).Several members of the basic region-leucine zipper (bZIP) class of transcription factors, including the CCAAT͞enhancer binding protein (C͞EBP) family have been implicated in the differentiation of hematopoietic cells (1-5). C͞EBP proteins have highly conserved bZIP C-terminal regions, but differ in their N-terminal regions (6, 7). A consensus site,

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The p50 subunit of NF-kappa B associates with the NF-IL6 transcription factor.

Cited by 303 publications

References 32 publications

An interaction between the DNA-binding domains of RelA(p65) and Sp1 mediates human immunodeficiency virus gene activation.

An interaction between the DNA-binding domains of RelA(p65) and Sp1 mediates human immunodeficiency virus gene activation.

Activation of the Mouse Ig Germline ε Promoter by IL-4 Is Dependent on AP-1 Transcription Factors

CCAAT/enhancer binding protein ɛ is preferentially up-regulated during granulocytic differentiation and its functional versatility is determined by alternative use of promoters and differential splicing

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