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Home > Curated Information Page > PubMed Id: 24703947
Wang H, et al. (2014) Mixed Lineage Kinase Domain-like Protein MLKL Causes Necrotic Membrane Disruption upon Phosphorylation by RIP3. Mol Cell 54, 133-46 24703947
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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T357-p - MLKL (human)
Modsite: FELRkTQtsMSLGTt SwissProt Entrez-Gene
Orthologous residues
MLKL (human): T357‑p, MLKL (mouse): N344‑p, MLKL (rat): T344‑p
Characterization
Methods used to characterize site in vivo immunoassay, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma, lymphoma
Relevant cell lines - cell types - tissues:  HeLa (cervical), HT-29 (intestinal), liver, U-937 (myeloid)
Cellular systems studied:  cell lines, tissue
Species studied:  human
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE RIPK3 (human) siRNA inhibition of enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
Z-VAD-FMK, TNF increase
Necrostatin-1 LPS, TNF, Z-VAD-FMK inhibit treatment-induced increase
LPS, Z-VAD-FMK increase
Downstream Regulation
Effect of modification (function):  intracellular localization, molecular association, regulation, protein conformation
Effect of modification (process):  apoptosis, induced
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
KDELC1 (human) Induces microscopy-colocalization
TOM20 (human) Induces microscopy-colocalization
LAMP1 (human) Induces microscopy-colocalization
Comments:  Liposome leakage

S358-p - MLKL (human)
Modsite: ELRkTQtsMSLGTtR SwissProt Entrez-Gene
Orthologous residues
MLKL (human): S358‑p, MLKL (mouse): S345‑p, MLKL (rat): S345‑p
Characterization
Methods used to characterize site in vivo immunoassay, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  colorectal cancer, colorectal carcinoma, lymphoma
Relevant cell lines - cell types - tissues:  HeLa (cervical), HT-29 (intestinal), liver, U-937 (myeloid)
Cellular systems studied:  cell lines, tissue
Species studied:  human
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE RIPK3 (human) siRNA inhibition of enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
Z-VAD-FMK, TNF increase
Necrostatin-1 LPS, TNF, Z-VAD-FMK inhibit treatment-induced increase
LPS, Z-VAD-FMK increase
Downstream Regulation
Effect of modification (function):  intracellular localization, molecular association, regulation, protein conformation
Effect of modification (process):  apoptosis, induced
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
LAMP1 (human) Induces microscopy-colocalization
KDELC1 (human) Induces microscopy-colocalization
TOM20 (human) Induces microscopy-colocalization
Comments:  Liposome leakage