Curated Information
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PubMed Id: 19734889 
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.
Melixetian M, Klein DK, Sørensen CS, Helin K (2009) NEK11 regulates CDC25A degradation and the IR-induced G2/M checkpoint. Nat Cell Biol 11, 1247-53 19734889
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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S76-p - Cdc25A (human) ▲
Orthologous residues
Cdc25A (human): S76‑p, Cdc25A iso2 (human): S76‑p, Cdc25A (mouse): S74‑p, Cdc25A (rat): S76‑p
Downstream Regulation
 Effect of modification (function):  phosphorylation
 Comments:  stimulates phosphorylation of S82 and S88 in vitro

S79-p - Cdc25A (human) ▲
Orthologous residues
Cdc25A (human): S79‑p, Cdc25A iso2 (human): S79‑p, Cdc25A (mouse): S77‑p, Cdc25A (rat): S79‑p
Characterization
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE NEK11 (human)
Downstream Regulation
 Effect of modification (function):  protein degradation, ubiquitination

S82-p - Cdc25A (human) ▲
Orthologous residues
Cdc25A (human): S82‑p, Cdc25A iso2 (human): S82‑p, Cdc25A (mouse): S80‑p, Cdc25A (rat): S82‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  HeLa (cervical), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE NEK11 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE NEK11 (human) siRNA inhibition of enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
siRNA decrease NEK11 siRNA
Downstream Regulation
 Effect of modification (function):  protein degradation, ubiquitination

S88-p - Cdc25A (human) ▲
Orthologous residues
Cdc25A (human): S88‑p, Cdc25A iso2 (human): S88‑p, Cdc25A (mouse): S86‑p, Cdc25A (rat): S88‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  HeLa (cervical), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE NEK11 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE NEK11 (human) siRNA inhibition of enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
siRNA decrease NEK11 siRNA
Downstream Regulation
 Effect of modification (function):  protein degradation, ubiquitination

S273-p - NEK11 (human) ▲
Orthologous residues
NEK11 (human): S273‑p, NEK11 iso4 (human): S273‑p, NEK11 (mouse): S274‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  bone cancer
 Relevant cell lines - cell types - tissues:  HeLa (cervical), U2OS (bone cell)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE Chk1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Chk1 (human) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
ionizing radiation increase
caffeine ionizing radiation inhibit treatment-induced increase
Go 6976 ionizing radiation inhibit treatment-induced increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced


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