Curated Information
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Curated Information Page
PubMed Id: 22195962 
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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Hitosugi T, et al. (2011) Tyrosine phosphorylation of mitochondrial pyruvate dehydrogenase kinase 1 is important for cancer metabolism. Mol Cell 44, 864-77 22195962
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.
Download Sites

S293-p - PDHA1 (human) ▲
Orthologous residues
PDHA1 (human): S293‑p, PDHA1 (mouse): S293‑p, PDHA1 (rat): S293‑p, PDHA1 (pig): S292‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  leukemia, acute myelogenous leukemia, lung cancer, non-small cell lung cancer
 Relevant cell lines - cell types - tissues:  KG1-A (myeloid), NCI-H1299 (pulmonary)
 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
TK1258 decrease
DCA increase
PDHK1 (human) increase PDHK1 shRNA inhibits
Downstream Regulation
 Comments:  S293D mutant resulted in decrease i n O2 consumption.

Y136-p - PDHK1 (human) ▲
Orthologous residues
PDHK1 (human): Y136‑p, PDHK1 (mouse): Y136‑p, PDHK1 (rat): Y136‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer, leukemia, acute myelogenous leukemia, chronic myelogenous leukemia, erythroid leukemia, lung cancer, non-small cell lung cancer, prostate cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), HEL (erythroid), K562 (erythroid), MDA-MB435 (breast cell), Molm 14 (myeloid), NCI-H1299 (pulmonary), PC3 (prostate cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE FGFR1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE FGFR1 (human) siRNA inhibition of enzyme, pharmacological inhibitor of upstream enzyme, co-immunoprecipitation, mutation in upstream enzyme recognition motif

Y243-p - PDHK1 (human) ▲
Orthologous residues
PDHK1 (human): Y243‑p, PDHK1 (mouse): Y241‑p, PDHK1 (rat): Y241‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer, leukemia, acute myelogenous leukemia, chronic myelogenous leukemia, erythroid leukemia, lung cancer, non-small cell lung cancer, prostate cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), HEL (erythroid), K562 (erythroid), MDA-MB435 (breast cell), Molm 14 (myeloid), NCI-H1299 (pulmonary), PC3 (prostate cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE FGFR1 (human)
KINASE FLT3 (human)
KINASE Abl (human)
KINASE JAK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE FGFR1 (human) siRNA inhibition of enzyme, pharmacological inhibitor of upstream enzyme, co-immunoprecipitation, mutation in upstream enzyme recognition motif
Downstream Regulation
 Effect of modification (function):  intracellular localization
 Comments:  localized to mitochondria in cancer cells

Y244-p - PDHK1 (human) ▲
Orthologous residues
PDHK1 (human): Y244‑p, PDHK1 (mouse): Y242‑p, PDHK1 (rat): Y242‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer, leukemia, acute myelogenous leukemia, chronic myelogenous leukemia, erythroid leukemia, lung cancer, non-small cell lung cancer, prostate cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), HEL (erythroid), K562 (erythroid), MDA-MB435 (breast cell), Molm 14 (myeloid), NCI-H1299 (pulmonary), PC3 (prostate cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE FGFR1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE FGFR1 (human) siRNA inhibition of enzyme, pharmacological inhibitor of upstream enzyme, co-immunoprecipitation, mutation in upstream enzyme recognition motif

Y136-p - PDHK1 (mouse) ▲
Orthologous residues
PDHK1 (human): Y136‑p, PDHK1 (mouse): Y136‑p, PDHK1 (rat): Y136‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer, leukemia, acute myelogenous leukemia, chronic myelogenous leukemia, erythroid leukemia, lung cancer, non-small cell lung cancer, prostate cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), HEL (erythroid), K562 (erythroid), MDA-MB435 (breast cell), Molm 14 (myeloid), NCI-H1299 (pulmonary), PC3 (prostate cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Downstream Regulation
 Effect of modification (function):  molecular association, regulation
 Effect of modification (process):  cell growth, induced
 Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
DLAT (human) Induces co-immunoprecipitation
 Comments:  Y to F mutants show decreased proliferation under hypoxia and increased oxidative phosphorylation.

Y241-p - PDHK1 (mouse) ▲
Orthologous residues
PDHK1 (human): Y243‑p, PDHK1 (mouse): Y241‑p, PDHK1 (rat): Y241‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer, leukemia, acute myelogenous leukemia, chronic myelogenous leukemia, erythroid leukemia, lung cancer, non-small cell lung cancer, prostate cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), HEL (erythroid), K562 (erythroid), MDA-MB435 (breast cell), Molm 14 (myeloid), NCI-H1299 (pulmonary), PC3 (prostate cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Downstream Regulation
 Effect of modification (process):  cell growth, induced
 Comments:  Y to F mutants show decreased proliferation under hypoxia and increased oxidative phosphorylation.

Y242-p - PDHK1 (mouse) ▲
Orthologous residues
PDHK1 (human): Y244‑p, PDHK1 (mouse): Y242‑p, PDHK1 (rat): Y242‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  breast cancer, leukemia, acute myelogenous leukemia, chronic myelogenous leukemia, erythroid leukemia, lung cancer, non-small cell lung cancer, prostate cancer
 Relevant cell lines - cell types - tissues:  A549 (pulmonary), HEL (erythroid), K562 (erythroid), MDA-MB435 (breast cell), Molm 14 (myeloid), NCI-H1299 (pulmonary), PC3 (prostate cell)
 Cellular systems studied:  cell lines
 Species studied:  human
Downstream Regulation
 Effect of modification (process):  cell growth, induced
 Comments:  Y to F mutants show decreased proliferation under hypoxia and increased oxidative phosphorylation.


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