Curated Information
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Home > Curated Information Page > PubMed Id: 29599132
Nguyen EK, et al. (2018) CaMKII (Ca/Calmodulin-Dependent Kinase II) in Mitochondria of Smooth Muscle Cells Controls Mitochondrial Mobility, Migration, and Neointima Formation. Arterioscler Thromb Vasc Biol 29599132
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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S91-p - MCU (mouse)
Modsite: VISVRLPsRRERCQF SwissProt Entrez-Gene
Orthologous residues
MCU (human): S92‑p, MCU iso2 (human): S92‑p, MCU iso3 (human): S43‑p, MCU (mouse): S91‑p, MCU (rat): S91‑p
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  VSMC
Cellular systems studied:  primary cells
Species studied:  mouse
Comments:  mitochondria mitoplasts
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CAMK2A (mouse) pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, phospho-antibody
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
PDGF increase
autocamtide_inhibitory_peptide PDGF inhibit treatment-induced increase