Curated Information
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Home > Curated Information Page > PubMed Id: 26317805
Song WJ, et al. (2015) Enhancement of BACE1 Activity by p25/Cdk5-Mediated Phosphorylation in Alzheimer's Disease. PLoS One 10, e0136950 26317805
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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T252-p - BACE (human)
Modsite: YTGSLWYtPIRREWY SwissProt Entrez-Gene
Orthologous residues
BACE (human): T252‑p, BACE (mouse): T252‑p, BACE (rat): T252‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mutation of modification site, phospho-antibody
Disease tissue studied:  adrenal cancer, pheochromocytoma, neuroblastoma
Relevant cell lines - cell types - tissues:  'neuron, hippocampal'-brain, brain, HEK293T (epithelial), PC-12 (chromaffin), SK-N-BE(2) (neural crest)
Cellular systems studied:  cell lines, tissue
Species studied:  human, mouse, rat
Enzymes shown to modify site in vitro
Type Enzyme
KINASE CDK5 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK5 (human) co-immunoprecipitation, transfection of wild-type enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
CDK5R1 (human) increase
seliciclib decrease
Downstream Regulation
Effect of modification (function):  activity, induced
Associated Diseases
Diseases Alterations Comments
Alzheimer's disease increased