Curated Information
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Home > Curated Information Page > PubMed Id: 19029119
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) activation of upstream enzyme, transfection of dominant-negative 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) activation of upstream enzyme, transfection of dominant-negative 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) activation of upstream enzyme, transfection of dominant-negative 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