JMY (L-16) Antibody: sc-10027

JMY Background Information
p300 and CBP (CREB-binding proteins) function as coactivators for various transcription factors, including p53. As cofactors, p300 and CBP possesses intrinsic acetyltransferase activity which may allow p300/CBP proteins to regulate transcription through direct acetylation and thereafter, enhance DNA binding activity. JMY is a nuclear cofactor for p300 that cooperatively enhances p53 activation in response to cellular stress. The p53 protein requires p300/CBP coactivator proteins in order to transcriptionally activate target genes. When p53 is activated, p300 component of the coactivator protein complexes associate with JMY and potentiate p53-dependent transcription and apoptosis. p53 acts as a sequence-specific transcription factor and upon stimulation, induces transcription of genes involved in growth arrest, including the waf1/cip1, bax, mdm2, and gadd45 genes. Disruption of p300 and JMY complexes inhibits p53-induced transcription of bax and blocks apoptosis. Due to alternative splicing, several isoforms of JMY are produced, and these various isoforms have different influencing affects on p53 activation, with some isoforms markedly enhancing p53 responses compared to the other splicing variants.