CREBP Mutation Schematic

Lab Report
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This paper investigates mutations in all domains of "3',5'-Cyclic Adenosine Monophosphate Response Element Binding" (CREB) (Brunetti, A, et al, 2000) transcriptional factor (TF) and its associated protein CBP that may result in Rubinstein-Taybi syndrome (RTS).


The kinase pathways, in essence, induce phosphorylation of a single residue SER133 (Salks Institute, Undated) on CREB to activate it. There is evidence of four such kinase pathways - cAMP-dependent protein kinase, multiple mitogen-activated protein kinases (MAPKs), ribosome S6 kinase and - and calmodulin-dependent kinases (CAMKs) (Euskirchen, G., et al, 2004). The phosphorylated CREB attracts coactivator CREB binding protein (CBP or CREBBP ) which allows the activated phosphorylated CREB to bind to cAMP-responsive element (CRE) sequences on DNA to initiate gene expression (Thiel, G., et al, 2005). CBP coactivator work is often copied by its paralog p300, a highly related transcriptional coactivator protein targeted by the adenoviral oncoprotein E1A (Brody, T.B., 1996). This is still not a very clear process as much has yet to be known about the mechanism by which CBP binds to the phosphorylated CREB and subsequently promotes gene transcription. For gene transcription to take place a polymerase complex must be recruited, it must then be subsequently isomerized and cleared to transcribe the target gene (Kim, J., et al, 2000). ...
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