Zheng M, et al. (2011) Inactivation of Rheb by PRAK-mediated phosphorylation is essential for energy-depletion-induced suppression of mTORC1. Nat Cell Biol 13, 263-72 21336308

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S130-p - RHEB (human) ▲

Modsite: LHMERVIsYEEGkAL SwissProt Entrez-Gene Orthologous residues RHEB (human): S130‑p, RHEB (mouse): S130‑p, RHEB (rat): S130‑p Characterization Methods used to characterize site in vivo:  [32P] ATP in vitro, immunoprecipitation, mass spectrometry (in vitro), mutation of modification site, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  293 (epithelial), E.coli (bacterial), MEF (fibroblast) Cellular systems studied:  cell lines Species studied:  bacteria, human, mouse Enzymes shown to modify site in vitro:  Type Enzyme KINASE MAPKAPK5 (mouse) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE MAPKAPK5 (human) co-immunoprecipitation, transfection of wild-type enzyme, siRNA inhibition of enzyme, transfection of inactive enzyme, genetic knockout/knockin of upstream enzyme, phospho-antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes 2-deoxyglucose increase acadesine increase Downstream Regulation Effect of modification (function):  activity, inhibited, phosphorylation Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Disrupts Comments:  reduce mTORC1 activity(S6K1 phosphorylation), disrupted Guanine nucleotide binding activity

T182-p - MAPKAPK5 (mouse) ▲

Modsite: VDQGDLMtPQFTPYY SwissProt Entrez-Gene Orthologous residues MAPKAPK5 (human): T182‑p, MAPKAPK5 iso2 (human): T182‑p, MAPKAPK5 (mouse): T182‑p, MAPKAPK5 (rat): T182‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  MEF (fibroblast) Cellular systems studied:  cell lines Species studied:  mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38B (mouse) transfection of wild-type enzyme, genetic knockout/knockin of upstream enzyme, phospho-antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes 2-deoxyglucose increase acadesine increase glucose_starvation increase Downstream Regulation Effect of modification (function):  phosphorylation Comments:  induces phosphorylation of RHEB