Lepore Signorile M, et al. (2023) Uncoupling p38α nuclear and cytoplasmic functions and identification of two p38α phosphorylation sites on β-catenin: implications for the Wnt signaling pathway in CRC models. Cell Biosci 13, 223 38041178

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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S111-p - CTNNB1 (human) ▲

Modsite: DEGMQIPstQFdAAH SwissProt Entrez-Gene Orthologous residues CTNNB1 (human): S111‑p, CTNNB1 (mouse): S111‑p, CTNNB1 (rat): S111‑p, CTNNB1 (rabbit): S111‑p Characterization Methods used to characterize site in vivo:  mass spectrometry (in vitro), mutation of modification site Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  HCT116 (intestinal) Cellular systems studied:  cell lines Species studied:  human Enzymes shown to modify site in vitro:  Type Enzyme KINASE P38A (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38A (human) co-immunoprecipitation, pharmacological inhibitor of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ralimetinib decrease Downstream Regulation Effect of modification (function):  molecular association, regulation Effect of modification (process):  signaling pathway regulation, transcription, induced Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Induces Comments:  regulates the Wnt signaling pathway

T112-p - CTNNB1 (human) ▲

Modsite: EGMQIPstQFdAAHP SwissProt Entrez-Gene Orthologous residues CTNNB1 (human): T112‑p, CTNNB1 (mouse): T112‑p, CTNNB1 (rat): T112‑p, CTNNB1 (rabbit): T112‑p Characterization Methods used to characterize site in vivo:  mass spectrometry (in vitro), mutation of modification site Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  HCT116 (intestinal) Cellular systems studied:  cell lines Species studied:  human Enzymes shown to modify site in vitro:  Type Enzyme KINASE P38A (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38A (human) co-immunoprecipitation, pharmacological inhibitor of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ralimetinib decrease Downstream Regulation Effect of modification (function):  molecular association, regulation Effect of modification (process):  signaling pathway regulation, transcription, induced Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays Induces Comments:  regulates the Wnt signaling pathway

T390-p - GSK3B (human) ▲

Modsite: RIQAAAstPtNAtAA SwissProt Entrez-Gene Orthologous residues GSK3B (human): T390‑p, GSK3B iso2 (human): T403‑p, GSK3B (mouse): P390‑p, GSK3B (rat): P390‑p, GSK3B (rabbit): T403‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  HCT116 (intestinal) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE P38A (human) genetic knockout/knockin of upstream enzyme, pharmacological inhibitor of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ralimetinib decrease Downstream Regulation Effect of modification (function):  enzymatic activity, inhibited