CBP and p300 are critical for normal embryonic development
Mouse models CBP and p300 are critical for normal embryonic development, as mice completely lacking either CBP or p300 protein, die at an early embryonic stage. In addition, mice
p300-CBP coactivator family – clinical significance
Mutations in CBP, and to a lesser extent p300, are the cause of Rubinstein-Taybi Syndrome, which is characterized by severe mental retardation. These mutations result in the loss
An example of a process involving p300 and CBP is G protein signaling
Function in G protein signaling Some G proteins stimulate adenylate cyclase that results in elevation of cAMP. cAMP stimulates PKA, which consists of four subunits, two regulat
p300 and CBP are thought to increase gene expression in three ways
Regulation of gene expression p300 and CBP are thought to increase gene expression in three ways: p300 regulates transcription by directly binding to transcription factor
p300-CBP coactivator family
The p300-CBP coactivator family in humans is composed of two closely related transcriptional co-activating proteins (or coactivators): Both p300 and CBP interact wit
Histone acetyltransferase p300
Histone acetyltransferase p300 also known as p300 HAT or E1A-associated protein p300 (where E1A = adenovirus early region 1A) also known as EP300 or p300 is an enzyme t
Rubinstein-Taybi Syndrome (RTS) is a rare genetic disorder that is the result of genetic mutations in either CBP or p300
Rubinstein-Taybi Syndrome (RTS) Type 1, which is caused by CBP mutations, for which over 500 different variations have been documented, accounts for approximately 55% of all cases