Curated Information
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PubMed Id: 21316606 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
Liu F, et al. (2011) JAK2V617F-mediated phosphorylation of PRMT5 downregulates its methyltransferase activity and promotes myeloproliferation. Cancer Cell 19, 283-94 21316606
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
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Y297-p - PRMT5 (human) ▲
Orthologous residues
PRMT5 (human): Y297‑p, PRMT5 (mouse): Y297‑p, PRMT5 (rat): Y297‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  bone cancer, leukemia, erythroid leukemia
 Relevant cell lines - cell types - tissues:  'hematopoietic progenitor, CD34+'-blood, 293T (epithelial), HEL (erythroid), HeLa (cervical), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JAK2 (human)
 Comments:  Jak2 V617F mutant kinase
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JAK2 (human) pharmacological inhibitor of upstream enzyme, co-immunoprecipitation, transfection of constitutively active enzyme Jak2 V617F mutant kinase
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
JAK inhibitor I decrease
CEP701 decrease
TG101348 decrease
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited, molecular association, regulation
 Effect of modification (process):  carcinogenesis, altered, cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
PRMT5 (human) Disrupts co-immunoprecipitation
 Comments:  contributes to the mutant Jak2 V617F -induced myeloproliferative phenotype; negatively regulates hematopoietic stem/progenitor cell expansion and erythroid differentiation

Y304-p - PRMT5 (human) ▲
Orthologous residues
PRMT5 (human): Y304‑p, PRMT5 (mouse): Y304‑p, PRMT5 (rat): Y304‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  bone cancer, leukemia, erythroid leukemia
 Relevant cell lines - cell types - tissues:  'hematopoietic progenitor, CD34+'-blood, 293T (epithelial), HEL (erythroid), HeLa (cervical), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JAK2 (human)
 Comments:  Jak2 V617F mutant kinase
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JAK2 (human) pharmacological inhibitor of upstream enzyme, co-immunoprecipitation, transfection of constitutively active enzyme Jak2 V617F mutant kinase
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
JAK inhibitor I decrease
CEP701 decrease
TG101348 decrease
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited, molecular association, regulation
 Effect of modification (process):  carcinogenesis, altered, cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
PRMT5 (human) Disrupts co-immunoprecipitation
 Comments:  contributes to the mutant Jak2 V617F -induced myeloproliferative phenotype; negatively regulates hematopoietic stem/progenitor cell expansion and erythroid differentiation

Y307-p - PRMT5 (human) ▲
Orthologous residues
PRMT5 (human): Y307‑p, PRMT5 (mouse): Y307‑p, PRMT5 (rat): Y307‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  bone cancer, leukemia, erythroid leukemia
 Relevant cell lines - cell types - tissues:  'hematopoietic progenitor, CD34+'-blood, 293T (epithelial), HEL (erythroid), HeLa (cervical), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE JAK2 (human)
 Comments:  Jak2 V617F mutant kinase
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JAK2 (human) pharmacological inhibitor of upstream enzyme, co-immunoprecipitation, transfection of constitutively active enzyme Jak2 V617F mutant kinase
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
JAK inhibitor I decrease
CEP701 decrease
TG101348 decrease
Downstream Regulation
 Effect of modification (function):  enzymatic activity, inhibited, molecular association, regulation
 Effect of modification (process):  carcinogenesis, altered, cell growth, altered
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
PRMT5 (human) Disrupts co-immunoprecipitation
 Comments:  contributes to the mutant Jak2 V617F -induced myeloproliferative phenotype; negatively regulates hematopoietic stem/progenitor cell expansion and erythroid differentiation


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