GSAP


Summary: Accumulation of neurotoxic amyloid-beta is a major hallmark of Alzheimer disease (AD; MIM 104300). Formation of amyloid-beta is catalyzed by gamma-secretase (see PSEN1; MIM 104311), a protease with numerous substrates. PION, or GSAP, selectively increases amyloid-beta production through a mechanism involving its interaction with both gamma-secretase and its substrate, the amyloid-beta precursor protein (APP; MIM 104760) C-terminal fragment (APP-CTF) (He et al., 2010 [PubMed 20811458]).[supplied by OMIM, Nov 2010].

NameOMIM IDEnsembl IDHGNC IDPHARMGKB IDMap Location
gamma-secretase activating proteinMIM:613552Ensembl:ENSG00000186088HGNC:HGNC:28042PA1647245007q11.23

GO terms in GSAP


Term TypeEvidence TypeGO Term IDGO Des.
BPIDAGO:0030162regulation of proteolysis
BPIDAGO:1902004positive regulation of amyloid-beta formation
CCIDAGO:0005802trans-Golgi network
MFIDAGO:0001540amyloid-beta binding
MFIPIGO:0005515protein binding

Gene expression in normal tissue: GSAP

Gene-model tissue-cancer distribution: Bubble Plot

Gene-drug pathway distribution

Pathways in GSAP


DatabasePathway IDPathway Des.

Gene-Drug: Aster Plot


Drug IDDrug NameModel Num.
iGMDRD353PD03259011

Gene in drug-gene network: Network Plot

Gene-drug targets distribution

Gene Structure: PDB

Models in GSAP

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