Pattingre S, et al. (2009) Role of JNK1-dependent Bcl-2 phosphorylation in ceramide-induced macroautophagy. J Biol Chem 284, 2719-28 19029119

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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T69-p - Bcl-2 (human) ▲

Modsite: SRDPVARtsPLQtPA SwissProt Entrez-Gene Orthologous residues Bcl‑2 (human): T69‑p, Bcl‑2 (mouse): T69‑p, Bcl‑2 (rat): T69‑p Characterization Methods used to characterize site in vivo:  mutation of modification site, western blotting Disease tissue studied:  breast cancer, colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  HeLa S3 (cervical), HT-29 (intestinal), MCF-7 (breast cell) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE JNK1 (human) transfection of dominant-negative enzyme, activation of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes C2-ceramide increase C2-DHCer no change compared to control Downstream Regulation Effect of modification (function):  molecular association, regulation Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays beclin 1 (human) Disrupts co-immunoprecipitation Comments:  induces autophagy

S70-p - Bcl-2 (human) ▲

Modsite: RDPVARtsPLQtPAA SwissProt Entrez-Gene Orthologous residues Bcl‑2 (human): S70‑p, Bcl‑2 (mouse): S70‑p, Bcl‑2 (rat): S70‑p Characterization Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  breast cancer, colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  HeLa S3 (cervical), HT-29 (intestinal), MCF-7 (breast cell) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE JNK1 (human) transfection of dominant-negative enzyme, activation of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes C2-ceramide increase C2-DHCer no change compared to control Downstream Regulation Effect of modification (function):  molecular association, regulation Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays beclin 1 (human) Disrupts co-immunoprecipitation Comments:  induces autophagy

S87-p - Bcl-2 (human) ▲

Modsite: AAAGPALsPVPPVVH SwissProt Entrez-Gene Orthologous residues Bcl‑2 (human): S87‑p, Bcl‑2 (mouse): S84‑p, Bcl‑2 (rat): S84‑p Characterization Methods used to characterize site in vivo:  mutation of modification site, western blotting Disease tissue studied:  breast cancer, colorectal cancer, colorectal carcinoma Relevant cell lines - cell types - tissues:  HeLa S3 (cervical), HT-29 (intestinal), MCF-7 (breast cell) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE JNK1 (human) transfection of dominant-negative enzyme, activation of upstream enzyme Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes C2-ceramide increase C2-DHCer no change compared to control Downstream Regulation Effect of modification (function):  molecular association, regulation Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays beclin 1 (human) Disrupts co-immunoprecipitation Comments:  induces autophagy

T183-p - JNK1 (human) ▲

Modsite: AGtsFMMtPyVVtRY SwissProt Entrez-Gene Orthologous residues JNK1 (human): T183‑p, JNK1 iso2 (human): T183‑p, JNK1 iso3 (human): T183‑p, JNK1 (mouse): T183‑p, JNK1 (rat): T183‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  HeLa S3 (cervical) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes C2-ceramide increase C2-DHCer no change compared to control

Y185-p - JNK1 (human) ▲

Modsite: tsFMMtPyVVtRYYR SwissProt Entrez-Gene Orthologous residues JNK1 (human): Y185‑p, JNK1 iso2 (human): Y185‑p, JNK1 iso3 (human): Y185‑p, JNK1 (mouse): Y185‑p, JNK1 (rat): Y185‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  HeLa S3 (cervical) Cellular systems studied:  cell lines Species studied:  human Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes C2-ceramide increase C2-DHCer no change compared to control