Curated Information
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Curated Information Page
PubMed Id: 18794806 
Nihira K, Taira N, Miki Y, Yoshida K (2008) TTK/Mps1 controls nuclear targeting of c-Abl by 14-3-3-coupled phosphorylation in response to oxidative stress. Oncogene 27, 7285-95 18794806
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, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
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T735-p - Abl (human)
Orthologous residues
Abl (human): T735‑p, Abl iso2 (human): T754‑p, Abl (mouse): T734‑p, Abl iso2 (mouse): T753‑p, Abl (rat): T734‑p, Abl iso2 (rat): T754‑p
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  HeLa (cervical)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE CLK4 (human)
KINASE TTK (human)
KINASE CLK1 (human)
KINASE MST1 (human)
KINASE MST2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE TTK (human) siRNA inhibition of enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
adriamycin no change compared to control
H2O2 increase
siRNA H2O2 TTK (human) inhibit treatment-induced increase
siRNA H2O2 CLK1 (human) no effect upon treatment-induced increase
siRNA H2O2 CLK4 (human) no effect upon treatment-induced increase
siRNA H2O2 MST1 (human) no effect upon treatment-induced increase
siRNA H2O2 MST2 (human) no effect upon treatment-induced increase
Downstream Regulation
 Effect of modification (function):  enzymatic activity, induced, intracellular localization
 Effect of modification (process):  apoptosis, inhibited

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