Fos and Jun bind cooperatively to the AP-1 site: reconstitution in vitro.

Rauscher, Frank J.; Voulalas, Pamela J.; Franza, B. R.; Curran, Tom

doi:10.1101/gad.2.12b.1687

Cited by 499 publications

(285 citation statements)

References 36 publications

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“…GCN4 and the mammalian AP-1, known at that time only as a transcription factor interacting with a specific enhancer sequence, share the same DNA binding specificity (Short, 1987;Haluska et al, 1988). Using this specific piece of DNA for affinity chromatography, the mammalian c-Jun was co-purified with c-Fos, marking the first identification of AP-1 as a heterodimer of c-Jun and c-Fos (Angel et al, 1988a;Harshman et al, 1988;Rauscher et al, 1988aRauscher et al, , 1988b.…”

Section: C-jun a Member Of The Ap-1 Complexmentioning

confidence: 99%

c-Jun, at the crossroad of the signaling network

2011

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Section: C-jun a Member Of The Ap-1 Complexmentioning

confidence: 99%

c-Jun, at the crossroad of the signaling network

2011

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“…We did not examine Fra-1 and Fra-2 Fos proteins in our study. It is very likely that c-Fos and FosB form heterodimers with c-Jun and JunD and activate the GL ⑀ promoter in vivo, because Fos proteins do not form homodimers but do heterodimerize with Jun proteins and because Fos/Jun heterodimers are more stable and have much higher DNA-binding affinities than Jun homodimers (25,44). In addition, we found that coexpressed c-Fos/JunD or FosB/JunD synergize with Stat6 to activate transcription, whereas overexpressed JunD alone does not (Figs.…”

Section: Ap-1 Is Required For Transcriptional Activation Of the Ig Glmentioning

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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“…These motifs are the AP1 site (CCTGGGTCAGC) at -149 -139, the MZF1 site (AATGGGGA) at -98 ~ -91, the SP1 site (CCTCGCCCA) at -80 --72, core sequences of Ets-1 binding site (GGAA) at -65 --62, and the AML1 binding site (TGTGGT) at -59 --54. The AP-1/jun family is the transcription activator that binds, in general, to the sequence TGACTCA found in enhancers of many cellular and viral genes [17]. MZF1 binding protein has previously been shown to be a transcription inhibitor of hematopoiesis-specific gene expression [18].…”

Section: The Promoter Structure Of Human Cr1 Genementioning

confidence: 99%

Characterization of the human CR1 gene promoter

1999

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Abbreviations: CR1, Complement receptor type 1; CR2, complement receptor type 2; DAF, decay accelerating factor; MCP, membrane cofactor protein; C4BR C4 binding protein,; DMSO, Dime@ sulfoxide; MMLV-RTase, Moloney murine lekemia virus reverse transcriptase; HPRT, hypoxanthine phosphoribosyltransferase. SUMMARY:The human CR1 is a single chain membrane glycoprotein that is a member of the group of regulators of the complement activation system. In order to clarify the regulatory mechanisms of human CR1 gene expression, the 5'-flanking region of the human CR1 gene was isolated and its promoter was characterized. The CR1 expression was found to be transcriptionally up-regulated in HL60 cells by stimulation with DMSO. The cloned CR1 gene promoter was sequenced and computer analyzed. The potential promoter region lacks a distinct TATA box sequence. The transcription initiation site was determined by primer extension and several possible regulatory elements for transcription were found in the promoter region.

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Fos and Jun bind cooperatively to the AP-1 site: reconstitution in vitro.

Cited by 499 publications

References 36 publications

c-Jun, at the crossroad of the signaling network

c-Jun, at the crossroad of the signaling network

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

Characterization of the human CR1 gene promoter

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