Curated Information
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Home > Curated Information Page > PubMed Id: 30858581
Zhao H, et al. (2019) AMPK-mediated activation of MCU stimulates mitochondrial Ca entry to promote mitotic progression. Nat Cell Biol 21, 476-486 30858581
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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S57-p - MCU (human)
Modsite: TVHQRIAsWQNLGAV SwissProt Entrez-Gene
Orthologous residues
MCU (human): S57‑p, MCU iso2 (human): S57‑p, MCU iso3 (human): S8‑p, MCU (mouse): S56‑p, MCU (rat): S56‑p
Characterization
Methods used to characterize site in vivo immunoassay, immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  bone cancer
Relevant cell lines - cell types - tissues:  E.coli (bacterial), HEK293T (epithelial), HeLa (cervical), U2OS (bone cell)
Cellular systems studied:  cell lines
Species studied:  bacteria, human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE AMPKA1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA1 (human) transfection of wild-type enzyme, pharmacological activator of upstream enzyme, phospho-antibody, co-immunoprecipitation, genetic knockout/knockin of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
DMSO no change compared to control
A-769662 increase
metformin increase
nocodazole increase Nocodazole-arrested
Downstream Regulation
Effect of modification (function):  activity, induced, intracellular localization
Effect of modification (process):  cell cycle regulation
Comments:  Regulates mitochondrial Ca2+ uptake and mitotic progression