adapter protein that forms a transcriptionally active complex with the gamma-secretase-derived amyloid precursor protein (APP) intracellular domain. Plays a central role in the response to DNA damage by translocating to the nucleus and inducing apoptosis. May act by specifically recognizing and binding histone H2AX phosphorylated on Y142 (H2AXpY142) at double-strand breaks (DSBs), recruiting other pro-apoptosis factors such as JNK1. Required for histone H4 acetylation at double-strand breaks (DSBs). Its ability to specifically bind modified histones and chromatin modifying enzymes such as TIP60, probably explains its trancription activation activity. Note: This description may include information from UniProtKB.
Protein type: Apoptosis; Transcription regulation; Adaptor/scaffold
Biological Process: axon guidance; extracellular matrix organization and biogenesis; positive regulation of DNA repair; transcription, DNA-dependent; positive regulation of apoptosis; apoptosis; positive regulation of transcription, DNA-dependent; neuron migration; negative regulation of thymidylate synthase biosynthetic process; signal transduction; negative regulation of neuron differentiation; axonogenesis; regulation of transcription, DNA-dependent; double-strand break repair; visual learning; positive regulation of transcription from RNA polymerase II promoter; negative regulation of cell growth; cell cycle arrest; response to DNA damage stimulus
Alt. Names/Synonyms: adaptor protein FE65a2; amyloid beta (A4) precursor protein-binding, family B, member 1 (Fe65); Amyloid beta A4 precursor protein-binding family B member 1; amyloid beta A4 precursor protein-binding, family B, member 1; APBB1; FE65; MGC:9072; Protein Fe65; RIR; stat-like protein
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.