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Literature summary for 3.4.23.46 extracted from

  • Cai, J.; Qi, X.; Kociok, N.; Skosyrski, S.; Emilio, A.; Ruan, Q.; Han, S.; Liu, L.; Chen, Z.; Bowes Rickman, C.; Golde, T.; Grant, M.B.; Saftig, P.; Serneels, L.; de Strooper, B.; Joussen, A.M.; Boulton, M.E.
    beta-Secretase (BACE1) inhibition causes retinal pathology by vascular dysregulation and accumulation of age pigment (2012), EMBO Mol. Med., 4, 980-991.
    View publication on PubMedView publication on EuropePMC
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Organism

Organism UniProt Comment Textmining
Mus musculus P56818
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Source Tissue

Source Tissue Comment Organism Textmining
neural retina highest expression Mus musculus
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General Information

General Information Comment Organism
physiological function BACE1-/- mice develop significant retinal pathology including retinal thinning, apoptosis, reduced retinal vascular density and an increase in the age pigment, lipofuscin. BACE1 expression is highest in the neural retina. Pigment epithelial-derived factor, a regulator of gamma-secretase, inhibits vascular endothelial growth factor-induced in vitro and in vivo angiogenesis and this is abolished by BACE1 inhibition. Intravitreal administration of BACE1 inhibitor or BACE1 small interfering RNA increases choroidal neovascularization in mice. BACE1 induces ectodomain shedding of vascular endothelial growth factor receptor VEGFR1 which is a prerequisite for gamma-secretase release of a 100 kDa intracellular domain. The increase in lipofuscin following BACE1 inhibition and RNAI knockdown is associated with lysosomal perturbations Mus musculus