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: Transcription regulation; Apoptosis; Adaptor/scaffold
Cellular Component: cell soma; cytoplasm; dendritic spine; growth cone; lamellipodium; nuclear speck; nucleoplasm; nucleus; perinuclear region of cytoplasm; plasma membrane; postsynaptic membrane; presynaptic membrane; protein complex; synapse
Molecular Function: beta-amyloid binding; chromatin binding; histone binding; protein binding; protein complex binding; tau protein binding; transcription factor binding
Biological Process: apoptosis; axonogenesis; cell cycle arrest; double-strand break repair; negative regulation of cell growth; negative regulation of thymidylate synthase biosynthetic process; positive regulation of apoptosis; positive regulation of DNA repair; positive regulation of protein secretion; positive regulation of transcription from RNA polymerase II promoter; positive regulation of transcription, DNA-dependent; regulation of transcription, DNA-dependent; response to DNA damage stimulus; response to iron ion; signal transduction; transcription, DNA-dependent
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.