Nuclear protein CBP is a coactivator for the transcription factor CREB

Kwok, Roland P.S.; Lundblad, James R.; Chrivia, John C.; Richards, Jane P.; Bächinger, Hans Peter; Brennan, Richard G.; Roberts, Stefan G. E.; Green, Michael R.; Goodman, Richard H.

doi:10.1038/370223a0

Cited by 1,384 publications

(1,037 citation statements)

References 19 publications

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“…The bromodomain appears to be highly conserved through evolution and is associated with many transcription factors having a role in histone acetylation including yeast and human GCN5 Candau et al, 1996;Georgakopoulos and Thireos, 1992;Wang et al, 1997), p300/CBP (Arany et al, 1994;Arias et al, 1994;Bannister and Kouzarides, 1996;Chrivia et al, 1993;Kwok et al, 1994;, pCAF and hTAF II 250 (Mizzen et al, 1996). It has, however, been shown by several groups that the bromodomain is dispensable for HAT activity Mizzen, 1996 #77;Ogryzko, 1996 #76).…”

Section: Discussionmentioning

confidence: 99%

“…CBP contains a bromodomain and has been implicated in the t(11;16) translocation with MLL and in the t(8;16) translocation with MOZ (Borrow et al, 1996). CBP has been shown to mediate the transcription of cyclic AMP response element (CRE) or mitogen responsive genes (Arias et al, 1994;Chrivia et al, 1993;Kwok et al, 1994) and interact with the basal transcription apparatus through TFIIB (Kwok et al, 1994). CBP or its close homologue, p300, can also interact with p300/CBP associated factor (P/CAF) which, as part of a protein complex is capable of histone acetylation .…”

Section: Discussionmentioning

confidence: 99%

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The cloning, mapping and expression of a novel gene, BRL, related to the AF10 leukaemia gene

McCullagh¹,

Chaplin²,

Meerabux³

et al. 1999

Oncogene

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The MLL gene is reciprocally translocated with one of a number of di erent partner genes in a proportion of human acute leukaemias. The precise mechanism of oncogenic transformation is unclear since most of the partner genes encode unrelated proteins. However, two partner genes, AF10 and AF17 are related through the presence of a cysteine rich region and a leucine zipper. The identi®cation of other proteins with these structures will aid our understanding of their role in normal and leukaemic cells. We report the cloning of a novel human gene (BRL) which encodes a protein containing a cysteine rich region related to that of AF10 and AF17 and is overall most closely related to the previously known protein BR140. BRL maps to chromosome 22q13 and shows high levels of expression in testis and several cell lines. The deduced protein sequence also contains a bromodomain, four potential LXXLL motifs and four predicted nuclear localization signals. A monoclonal antibody raised to a BRL peptide sequence con®rmed its widespread expression as a 120 Kd protein and demonstrated localization to the nucleus within spermatocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The cloning, mapping and expression of a novel gene, BRL, related to the AF10 leukaemia gene

McCullagh¹,

Chaplin²,

Meerabux³

et al. 1999

Oncogene

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“…CREB binding protein (CBP) and the closely related coactivator p300 (collectively referred to as CBP/p300) have been shown to cooperate with a variety of transcriptional activating proteins to regulate speci®c gene transcription (Kwok et al, 1994;Lundblad et al, 1995;Arany et al, 1994;Arias et al, 1994). In particular, Bannister and Kouzarides (1995) showed that CBP directly interacted with c-Fos in vitro and could stimulate GAL4-Fos transactivation in vivo.…”

Section: Introductionmentioning

confidence: 99%

The retinoblastoma gene family members pRB and p107 coactivate the AP-1-dependent mouse tissue factor promoter in fibroblasts

et al. 2000

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Serum-stimulation of quiescent mouse ®broblasts results in transcriptional activation of tissue factor (TF), the cellular initiator of blood coagulation. This requires the rapid entry of c-Fos into speci®c AP-1 DNA-binding complexes and can be strongly inhibited by the adenovirus E1A 12S gene product. In this study, we utilized a panel of E1A mutants de®cient in cellular protein binding to analyse the molecular basis for E1A inhibition of a minimal, c-Fos-dependent TF promoter/ reporter construct in mouse AKR-2B ®broblasts. Mutations which impaired binding of the retinoblastoma tumor suppressor protein family members pRB, p107, and p130 relieved E1A-mediated inhibition of transcription in response to serum-stimulation or c-Fos overexpression. Inhibition was restricted to the G 0 to G 1 transition, consistent with the speci®city of E1A for hypophosphorylated forms of RB proteins. Although E1A mutants de®cient in CBP/p300 binding retained the ability to inhibit TF transcription, deletion of the aminoterminal portion of the CBP/p300 interaction domain was required to permit rescue of TF promoter activity by coexpression of pRB. Moreover, ectopic p107 could e ectively substitute for pRB in relieving E1A-mediated repression. In primary mouse embryo ®broblasts, activity of the minimal AP-1-dependent TF promoter was suppressed in Rb 7/7 cells compared to parallel Rb +/7 and Rb +/+ transfectants. Ectopic expression of either pRB or p107 markedly enhanced TF promoter activity in Rb 7/7 ®broblasts. Collectively, these data imply that pRB and p107 can cooperate with c-Fos to activate TF gene transcription in ®broblasts and suggest a requirement for another, as yet unidenti®ed, E1A-binding protein. Oncogene (2000) 19, 3352 ± 3362.

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“…CBP was originally reported as a coactivator of CREB (Chrivia et al, 1993;Kwok et al, 1994), however it turned out to be a multifunctional co-activator of various transcription factors, including c-Myb and GATA-1 (Blobel et al, 1998;Dai et al, 1996;Mink et al, 1997;Oelgeschlager et al, 1996). In this study, we reveal the inhibitory interaction of cMyb and GATA-1, which is probably mediated by CBP.…”

Section: Introductionmentioning

confidence: 57%

Inhibitory interaction of c-Myb and GATA-1 via transcriptional co-activator CBP

et al. 2000

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Gene targeting experiments have revealed that transcription factors such as c-Myb and GATA-1 play crucial roles during hematopoietic di erentiation. c-Myb is necessary in the immature cells of almost every hematopoietic lineage and GATA-1 is essential for the development of the erythroid lineage. In addition, CREB-binding protein (CBP) acts as a transcriptional adapter for various transcription factors, including cMyb and GATA-1. In this paper, we show that the transcription factors c-Myb and GATA-1 each inhibit the transcriptional activity of the other and that any possible bipartite complexes c-Myb, GATA-1, and CBP could be formed, but the tripartite complex was hardly formed. The exclusive binding of GATA-1 and c-Myb to CBP is probably the molecular basis for the mutual inhibition of their transcriptional activity. Our data suggest that cross-talk between these three factors might be important for hematopoietic di erentiation and that CBP functions as a key molecule during the process.

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Nuclear protein CBP is a coactivator for the transcription factor CREB

Cited by 1,384 publications

References 19 publications

The cloning, mapping and expression of a novel gene, BRL, related to the AF10 leukaemia gene

The cloning, mapping and expression of a novel gene, BRL, related to the AF10 leukaemia gene

The retinoblastoma gene family members pRB and p107 coactivate the AP-1-dependent mouse tissue factor promoter in fibroblasts

Inhibitory interaction of c-Myb and GATA-1 via transcriptional co-activator CBP

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