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amyloid beta A4 protein-binding family B member 1; protein Fe65 (APBB1 FE65 RIR)

Function: - binds to intracellular domain of APP - Fe65 binds C-terminal region of APP - after cleavage of APP by APP gamma secretase, carries APP C-terminus to nucleus - Fe65 also binds to the cytolasmic domain of LRP1 - plays a central role in the response to DNA damage by translocating to the nucleus & inducing apoptosis - may act by specifically recognizing & binding histone H2AX phosphorylated on Tyr-142 (H2AXY142ph) at DNA double-strand breaks), recruiting other pro-apoptosis factors such as MAPK8/JNK1 - required for histone H4 acetylation at DNA double-strand breaks - ability to specifically bind modified histones & chromatin modifying enzymes such as KAT5/TIP60, probably explains its trancription activation activity - phosphorylated following nuclear translocation - phosphorylation at Tyr-546 enhances the transcription activation activity & reduces the affinity with RASD1/DEXRAS1 - component of a complex, at least composed of APBB1, RASD1/DEXRAS1 & APP - interacts (via PID domain 2) with APP (with the intracellular domain of the beta-amyloid precursor protein) - interacts (via PID domain 2) with RASD1/DEXRAS1; impairs the trancription activation activity - interacts (via PID domain 1) with KAT5/TIP60 - interacts (via the WW domain) with the proline-rich region of APBB1IP (putative) - interacts (via the WW domain) with histone H2AX (when phosphorylated on Tyr-142) & the proline-rich region of ENAH - interacts with MAPK8 Structure: - contains 2 PID domains - contains 1 WW domain Compartment: - cell membrane, cytoplasm, nucleus - in normal conditions, it mainly localizes to the cytoplasm, - a small fraction is tethered to the cell membrane via its interaction with APP - following exposure to DNA damaging agents, it is released from cell membrane & translocates to the nucleus - nuclear translocation is under the regulation of APP Alternative splicing: named isoforms=2 Expression: highly expressed in brain Polymorphism: - polymorphisms carry susceptibility to late onset Alzheimer's disease Pathology: - mutations in Fe65 affect the ability of animals to forget

Interactions

molecular events

General

amyloid beta A4 precursor protein binding family phosphoprotein

Properties

SIZE: entity length = 710 aa MW = 77 kD COMPARTMENT: cytoplasm cell nucleus MOTIF: glutamate-rich region {158-171} MOTIF: glutamate residue (SEVERAL) WW domain (W/rsp5/WWP domain) {253-285} phosphotyrosine interaction domain NAME: phosphotyrosine interaction domain SITE: 370-509 phosphotyrosine interaction domain NAME: phosphotyrosine interaction domain SITE: 542-699 MOTIF: Tyr phosphorylation site {Y546}

Database Correlations

OMIM 602709 UniProt O00213 PFAM correlations Entrez Gene 322 Kegg hsa:322

References

  1. Cao X, Sudhof TC. A transcriptionally [correction of transcriptively] active complex of APP with Fe65 and histone acetyltransferase Tip60. Science. 2001 Jul 6;293(5527):115-20. Erratum in: Science 2001 Aug 24;293(5534):1436. PMID: 11441186
  2. Entrez Gene :accession 322

Component-of

molecular complex