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Orthologous residues
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PKM2 (human): Y105‑p, PKM2 iso2 (human): Y105‑p, PKM2 iso3 (human): Y179‑p, PKM2 (mouse): Y105‑p, PKM2 (rat): Y105‑p, PKM2 iso2 (rat): Y105‑p
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Characterization
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Methods used to characterize site in vivo:
mass spectrometry, mutation of modification site, phospho-antibody, western blotting
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Disease tissue studied:
breast cancer, leukemia, acute myelogenous leukemia, chronic myelogenous leukemia, erythroid leukemia, lung cancer, non-small cell lung cancer, prostate cancer
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Relevant cell lines - cell types - tissues:
293T (epithelial) [FGFR1 (human), transfection], A549 (pulmonary), BaF3 ('B lymphocyte, precursor') [FGFR1 (human), transfection], DU 145 (prostate cell), HEL (erythroid), K562 (erythroid), KG-1a, MDA-MB231 (breast cell), MO-91 (myeloid), Molm 14 (myeloid), NCI-H1299 (pulmonary) [FGFR1 (human), transfection], PC3 (prostate cell)
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Cellular systems studied:
cell lines
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Species studied:
human, mouse
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Comments:
constitutively active ZNF198-FGFR1 transfected cells
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Enzymes shown to modify site in vitro:
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Upstream Regulation
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Potential in vivo enzymes for site:
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Type
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Enzyme
|
Evidence
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Notes
|
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KINASE
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FGFR1 (human)
|
pharmacological inhibitor of upstream enzyme
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|
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Treatments, proteins and their effect on site modification:
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|
Treatments
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Referenced Treatments
|
Manipulated Protein
|
Referenced Protein
|
Effect
|
Notes
|
|
imatinib
|
|
|
|
decrease
|
|
|
AG490
|
|
|
|
decrease
|
|
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TKI258
|
|
|
|
decrease
|
|
|
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Downstream Regulation
|
|
Effect of modification (function):
enzymatic activity, inhibited, molecular association, regulation
|
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Effect of modification (process):
carcinogenesis, induced, cell growth, altered
|
|
Modification regulates interactions with:
|
|
Interacting molecule
|
Interacting domains
|
Effect
|
Consequences (function)
|
Consequences (process)
|
Detection assays
|
|
PKM2 (human)
|
|
Disrupts
|
|
|
chemical cross-linking
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|
|
Comments:
disrupts tetramerization of PKM2
|
