Curated Information
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Home > Curated Information Page > PubMed Id: 29074724
Qian X, et al. (2018) Conversion of PRPS Hexamer to Monomer by AMPK-Mediated Phosphorylation Inhibits Nucleotide Synthesis in Response to Energy Stress. Cancer Discov 8, 94-107 29074724
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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S180-p - PRPS1 (human)
Modsite: GGAkRVTsIADrLNV SwissProt Entrez-Gene
Orthologous residues
PRPS1 (human): S180‑p, PRPS1 (mouse): S180‑p, PRPS1 (rat): S180‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  brain cancer, glioblastoma, glioma, breast cancer, liver cancer, hepatocellular carcinoma, lung cancer, non-small cell lung cancer, non-small cell lung adenocarcinoma, pancreatic cancer, pancreatic carcinoma
Relevant cell lines - cell types - tissues:  A549 (pulmonary), BxPC-3 (pancreatic), HEK293T (epithelial), Hep 3B2.1-7 (hepatic), Huh7 (hepatic), MDA-MB-231 (breast cell), U87MG (glial)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE AMPKA1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA1 (human) pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, pharmacological activator of upstream enzyme, co-immunoprecipitation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
hypoxia increase
compound_C hypoxia inhibit treatment-induced increase
Downstream Regulation
Effect of modification (function):  activity, inhibited, protein conformation
Effect of modification (process):  cell growth, inhibited
Comments:  converts PRPS1/2 hexamers to monomers; tumor cell growth inhibited

S180-p - PRPS2 (human)
Modsite: GGAkRVTsIADrLNV SwissProt Entrez-Gene
Orthologous residues
PRPS2 (human): S180‑p, PRPS2 iso2 (human): S183‑p, PRPS2 (mouse): S180‑p
Characterization
Methods used to characterize site in vivo immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  brain cancer, glioblastoma, glioma, breast cancer, liver cancer, hepatocellular carcinoma, lung cancer, non-small cell lung cancer, non-small cell lung adenocarcinoma, pancreatic cancer, pancreatic carcinoma
Relevant cell lines - cell types - tissues:  A549 (pulmonary), BxPC-3 (pancreatic), HEK293T (epithelial), Hep 3B2.1-7 (hepatic), Huh7 (hepatic), MDA-MB-231 (breast cell), U87MG (glial)
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE AMPKA1 (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE AMPKA1 (human) pharmacological inhibitor of upstream enzyme, activation of upstream enzyme, pharmacological activator of upstream enzyme, co-immunoprecipitation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
hypoxia increase
compound_C hypoxia inhibit treatment-induced increase
Downstream Regulation
Effect of modification (function):  activity, inhibited, protein conformation
Effect of modification (process):  cell growth, inhibited
Comments:  converts PRPS1/2 hexamers to monomers; tumor cell growth inhibited