Song H, et al. (2016) Stress-induced nuclear translocation of CDK5 suppresses neuronal death by downregulating ERK activation via VRK3 phosphorylation. Sci Rep 6, 28634 27346674

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.

Click on the protein name to open the protein page, and on the RSD number to open the site page.

Download

S108-p - VRK3 (human) ▲

Modsite: RPPtPKssPQKtRKs SwissProt Entrez-Gene Orthologous residues VRK3 (human): S108‑p, VRK3 iso2 (human): S108‑p, VRK3 (mouse): S108‑p, VRK3 iso3 (mouse): ‑, VRK3 (rat): S108‑p Characterization Methods used to characterize site in vivo:  immunoassay, mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  neuroblastoma Relevant cell lines - cell types - tissues:  'neuron, cortical'-brain, brain, SH-SY5Y (neural crest) Cellular systems studied:  cell lines, primary cultured cells, tissue Species studied:  human, mouse 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) modification site within consensus motif, co-immunoprecipitation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes H2O2 increase Downstream Regulation Effect of modification (function):  enzymatic activity, induced, intracellular localization, molecular association, regulation Effect of modification (process):  apoptosis, inhibited Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays ERK2 (human) Induces phosphorylation pull-down assay Comments:  recruitment of phospho-ERK to VHR, VHR phosphatase activity increased, increased Bak and Bax expression, Associated Diseases Diseases Alterations Comments Parkinson's disease, Alzheimer's disease increased

S115-p - VRK3 (human) ▲

Modsite: sPQKtRKsPQVtRGs SwissProt Entrez-Gene Orthologous residues VRK3 (human): S115‑p, VRK3 iso2 (human): S115‑p, VRK3 (mouse): ‑, VRK3 iso3 (mouse): ‑, VRK3 (rat): S115‑p Characterization Methods used to characterize site in vivo:  mutation of modification site Disease tissue studied:  neuroblastoma Relevant cell lines - cell types - tissues:  SH-SY5Y (neural crest) Cellular systems studied:  cell lines Species studied:  human

S122-p - VRK3 (human) ▲

Modsite: sPQVtRGsPQKtSCs SwissProt Entrez-Gene Orthologous residues VRK3 (human): S122‑p, VRK3 iso2 (human): S122‑p, VRK3 (mouse): ‑, VRK3 iso3 (mouse): ‑, VRK3 (rat): ‑ Characterization Methods used to characterize site in vivo:  mutation of modification site Disease tissue studied:  neuroblastoma Relevant cell lines - cell types - tissues:  SH-SY5Y (neural crest) Cellular systems studied:  cell lines Species studied:  human

S129-p - VRK3 (human) ▲

Modsite: sPQKtSCsPQKTRQs SwissProt Entrez-Gene Orthologous residues VRK3 (human): S129‑p, VRK3 iso2 (human): S129‑p, VRK3 (mouse): ‑, VRK3 iso3 (mouse): ‑, VRK3 (rat): ‑ Characterization Methods used to characterize site in vivo:  mutation of modification site Disease tissue studied:  neuroblastoma Relevant cell lines - cell types - tissues:  SH-SY5Y (neural crest) Cellular systems studied:  cell lines Species studied:  human

S136-p - VRK3 (human) ▲

Modsite: sPQKTRQsPQTLKRS SwissProt Entrez-Gene Orthologous residues VRK3 (human): S136‑p, VRK3 iso2 (human): S136‑p, VRK3 (mouse): S115‑p, VRK3 iso3 (mouse): ‑, VRK3 (rat): ‑ Characterization Methods used to characterize site in vivo:  mutation of modification site Disease tissue studied:  neuroblastoma Relevant cell lines - cell types - tissues:  SH-SY5Y (neural crest) Cellular systems studied:  cell lines Species studied:  human