CREB-binding Protein and p300 in Transcriptional Regulation*
By Ngan K. Vo, R. Goodman. Journal of Biological Chemistry, 2001
890 citations recorded by the source corpus.
CREB-binding protein (CBP) and p300 are believed to participate in the activities of hundreds of different transcription factors (see Fig. 1). Current models suggest that the binding of these coactivators to transcription factor activation domains positions histone acetyltransferases (HATs) near specific nucleosomes in target gene promoter regions (for review, see Ref. 1). Interactions with components of the general transcriptional machinery, such as TFIID, TFIIB, and the RNA polymerase II holoenzyme (RNAPII) have also been suggested to contribute to CBP/p300 function. The simultaneous interaction of multiple transcription factors with CBP/p300 has been proposed to contribute to transcriptional synergy. Conversely, competition for CBP/p300 binding has been suggested to mediate some examples of signal-induced transcriptional repression. An overview of CBP/p300 in cellular growth and differentiation has recently been published (2), but many questions regarding their role in transcriptional regulation remain unanswered. This review deals with some of the more controversial aspects of CBP/p300 function. In particular, we will ask whether CBP and p300 have distinct functions, review the evidence for their regulation by phosphorylation, and ask whether they function primarily by acetylating histones or other proteins. We will also revisit the evidence for the role of CBP/p300 as transcriptional “integrators.” Finally, we will attempt to localize CBP/p300 function within the complex series of processes involved in transcriptional activation.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/910851ceedaf4bd90964bb0e8f4871fcf78663cb
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Citations in the corpus
- Overview of Nomenclature of Nuclear Receptors (2006, background): “The p160 family of proteins, cAMP response element-binding protein (CBP), and p300 are considered to be among the first recruited by activated NRs (Chen et al., 2000; Vo and Goodman, 2001; McKenna and O’Malley, 2002).”
- Mechanisms of tamoxifen resistance. (2004, background): “Other coactivators include the SWI/ SNF complexes, CREB-binding protein (CBP), p300/ CBP-associated factor (PCAF), and the TRAP/DRIP/ SMCC complex (Chen et al. 1997, Sudarsanam & Winston 2000, Ito & Roeder 2001, Vo & Goodman 2001).”
- Wired for reproduction: organization and development of sexually dimorphic circuits in the mammalian forebrain. (2002, background): “In addition to CREB, CBP has binding sites for a wide variety of transcription factors including Fos and Jun (Vo & Goodman 2001).”
- Nuclear retinoid receptors and the transcription of retinoid-target genes. (2004, background): “Other coactivators, p300/CBP (Vo and Goodman, 2001) and CARM-1 (Chen et al.”
- How do lncRNAs regulate transcription? (2017, background): “p300/CBP p300 and CBP [cyclic adenosine monophosphate response element– binding protein (CREB)–binding protein] are two highly homologous and conserved proteins that have intrinsic HAT activity, which plays a critical role in regulating gene expression through lysine acetylation of histone H3 (94).”