Li D, et al. (2020) Casein kinase 1G2 suppresses necroptosis-promoted testis aging by inhibiting receptor-interacting kinase 3. Elife 9 33206046

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S211-p - CK1G2 (mouse) ▲

Modsite: IPYREHKsLTGtARY SwissProt Entrez-Gene Orthologous residues CK1G2 (human): S211‑p, CK1G2 (mouse): S211‑p, CK1G2 (rat): S211‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mass spectrometry, mutation of modification site Relevant cell lines - cell types - tissues:  HEK293T (epithelial), Leydig, MEF (fibroblast), sertoli-testis, spermatocytes Cellular systems studied:  cell lines Species studied:  human, mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE CK1G2 (mouse) Comments:  autophosphorylation Downstream Regulation Effect of modification (function):  molecular association, regulation, phosphorylation Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays RIPK3 (human) Induces enzymatic activity, inhibited, phosphorylation, molecular association, regulation co-immunoprecipitation Comments:  inhibits phosphorylation of MLKL, binding to RIPK3 inhibits RIPK3 binding to RIPK1

T215-p - CK1G2 (mouse) ▲

Modsite: EHKsLTGtARYMSIN SwissProt Entrez-Gene Orthologous residues CK1G2 (human): T215‑p, CK1G2 (mouse): T215‑p, CK1G2 (rat): T215‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mass spectrometry, mutation of modification site Relevant cell lines - cell types - tissues:  HEK293T (epithelial), Leydig, MEF (fibroblast), sertoli-testis, spermatocytes Cellular systems studied:  cell lines Species studied:  human, mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE CK1G2 (mouse) Comments:  autophosphorylation Downstream Regulation Effect of modification (function):  molecular association, regulation, phosphorylation Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays RIPK3 (human) Induces enzymatic activity, inhibited, phosphorylation, molecular association, regulation co-immunoprecipitation Comments:  inhibits phosphorylation of MLKL, binding to RIPK3 inhibits RIPK3 binding to RIPK1

S345-p - MLKL (mouse) ▲

Modsite: ELSKTQNsIsRtAKS SwissProt Entrez-Gene Orthologous residues MLKL (human): S358‑p, MLKL (mouse): S345‑p, MLKL iso2 (mouse): S345‑p, MLKL (rat): S345‑p Characterization Methods used to characterize site in vivo:  immunoassay, phospho-antibody, western blotting Disease tissue studied:  colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  HEK293T (epithelial), HT-29 (intestinal), MEF (fibroblast), testis Cellular systems studied:  cell lines, tissue Species studied:  human, mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE RIPK3 (mouse) 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 TRAIL, Z-VAD-FMK increase TNF, Z-VAD-FMK increase LPS, Z-VAD-FMK increase LPS, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments TNF, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments TRAIL, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments development CK1G2 (mouse) increase CK1G2 KO CK1G2 (mouse) decrease CK1G2 KO increases RIPK3 (mouse) CK1G2 (mouse) inhibit treatment-induced decrease RIPK3 KO augments development increase

T231-p - RIPK3 (mouse) ▲

Modsite: EAELVDKtsLIRETV SwissProt Entrez-Gene Orthologous residues RIPK3 (human): P226‑p, RIPK3 (mouse): T231‑p, RIPK3 (rat): T228‑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:  HEK293T (epithelial), HT-29 (intestinal), MEF (fibroblast) Cellular systems studied:  cell lines Species studied:  human, mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes TRAIL, Z-VAD-FMK increase TNF, Z-VAD-FMK increase LPS, Z-VAD-FMK increase LPS, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments TNF, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments TRAIL, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments

S232-p - RIPK3 (mouse) ▲

Modsite: AELVDKtsLIRETVC SwissProt Entrez-Gene Orthologous residues RIPK3 (human): S227‑p, RIPK3 (mouse): S232‑p, RIPK3 (rat): S229‑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:  HEK293T (epithelial), HT-29 (intestinal), MEF (fibroblast) Cellular systems studied:  cell lines Species studied:  human, mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE RIPK3 (mouse) Comments:  autophosphorylation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes CK1D (mouse) decrease CK1E (mouse) decrease CK1G2 (mouse) decrease CK1A (mouse) no change compared to control CK1G1 (mouse) no change compared to control CK2A1 (mouse) no change compared to control CK2A2 (mouse) no change compared to control CK2B (mouse) no change compared to control TRAIL, Z-VAD-FMK increase TNF, Z-VAD-FMK increase LPS, Z-VAD-FMK increase LPS, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments TNF, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments TRAIL, Z-VAD-FMK CK1G2 (mouse) inhibit treatment-induced increase CK1G2 KO augments Downstream Regulation Effect of modification (function):  phosphorylation Comments:  induces phosphorylation of MLKL