Purified transcription factor AP-1 interacts with TPA-inducible enhancer elements

Lee, Wes; Mitchell, Pamela J.; Tjian, Robert

doi:10.1016/0092-8674(87)90612-x

Cited by 1,986 publications

(951 citation statements)

References 49 publications

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“…It has been shown that tumor promoter phorbol-ester (TPA), growth factors or stress stimuli can significantly enhance the DNA binding and transcription activity of c-Jun (Lee et al, 1987;Quantin and Breathnach, 1988;Pertovaara et al, 1989;Sherman et al, 1990;Devary et al, 1991). Initiation of this process begins with stimulus activated signal transduction cascades that lead to a rapid change in the phosphorylation state of c-Jun.…”

Section: C-jun Expression and Activitymentioning

confidence: 99%

c-Jun, at the crossroad of the signaling network

2011

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Section: C-jun Expression and Activitymentioning

confidence: 99%

c-Jun, at the crossroad of the signaling network

2011

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“…We therefore examined binding of nuclear proteins from HeLa tk 7 cells to the p53-AP-1 motif in comparison with the coll-TRE in gel retardation assays after antibody perturbation with anti c-Fos or anti c-Jun antibodies ( Figure 3). Prior to the preparation of the nuclear extracts, the HeLa tk 7 cells were treated with TPA for 24 h to activate the AP-1 (Lee et al, 1987, Angel et al, 1987, Lamph et al, 1988 and NF-kB (Sen andBaltimore, 1986, Bohnlein et al, 1988) transcription factors. Up to ®ve shifted complexes appeared in case of the putative AP-1 motif from the hp53-promoter (complexes`a ± e' in Figure 3a).…”

Section: Comparison Of the Human And Mouse P53 Promotersmentioning

confidence: 99%

Expression of human p53 requires synergistic activation of transcription from the p53 promoter by AP-1, NF-κB and Myc/Max

et al. 1999

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Transcriptional control of p53 expression participates in the generation of appropriate levels of active p53 in response to mitogenic stimulation. This prompted us to study the role of a putative AP-1 and a NF-kB motif in the human p53 promoter for transcriptional regulation. We show that mutation of the AP-1 or the NF-kB motif abolishes transcription from the human p53 promoter in HeLa, HepG2 and adenovirus type 5 E1-transformed 293 cells. In comparison, mutation of the previously characterized Myc/Max/USF binding site in the human p53 promoter reduces the transcription rate ®vefold. The AP-1 motif in the human p53 promoter binds c-Fos and c-Jun and the NF-kB motif binds p50 NF-kB1 and p65 RelA . The cooperative nature of transcriptional activation by these factors was documented by repression of c-fos or NF-kB1 translation: Pretreatment of the cells with a cfos or p50 NF-kB1 antisense oligonucleotide suppresses transcription from the human p53 promoter completely. In addition, we show that (a) the level of endogenous p53 mRNA and (b) transcription from the strictly p53-dependent human mdm2 promoter are reduced in the presence of c-fos, c-jun, p50 NF-kB1 , p65 RelA or c-myc antisense oligonucleotides, underscoring the importance of these transcription factors for the expression of functional p53.

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“…labelled with the Klenow fragment of DNA polymerase 1 as described [3], was then added (0.2-0.6 ng, ca 20 000 cpm) and incubation was continued for 30 min at room tempcraturc, Electrophoresis was performed on 4% polyacrylamide gels in Tris-borate, pH 7.6, [3] at 12.5 V/cm for 2.5 h at 4°C. Footprint assays were performed as described [6] but with the incubation conditions of the bandshift experiments,…”

Section: Bandsir@ and Dnase I Foorprinf Assaysmentioning

confidence: 99%

Regions in the promoter of the yeast FBP1 gene implicated in catabolite repression may bind the product of the regulatory gene MIG1

1991

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We have identified in the promoter of the yeast FBPl gene two sites able to bind nuclear proteins. These sites have a nucleotide sequence strongly similar to that of sites which bind the regulatory protein MIGl in the promoters of GAL4 and SUCZ. Deletions performed in the FBPI promoter showed that one of the sites contributes to catabolite repression of this gene. In the same promoter, another region was identified with a strong effect on the catabolite repression of FBPI. In this region a sequence similar to the consensus for the binding site of the MIGl protein was also present.

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Purified transcription factor AP-1 interacts with TPA-inducible enhancer elements

Cited by 1,986 publications

References 49 publications

c-Jun, at the crossroad of the signaling network

c-Jun, at the crossroad of the signaling network

Expression of human p53 requires synergistic activation of transcription from the p53 promoter by AP-1, NF-κB and Myc/Max

Regions in the promoter of the yeast FBP1 gene implicated in catabolite repression may bind the product of the regulatory gene MIG1

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