Curated Information
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Curated Information Page
PubMed Id: 16984892 
Wang SY, Iordanov M, Zhang Q (2006) c-Jun NH2-terminal kinase promotes apoptosis by down-regulating the transcriptional co-repressor CtBP. J Biol Chem 281, 34810-5 16984892
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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S422-p - CtBP1 (human)
Orthologous residues
CtBP1 (human): S422‑p, CtBP1 iso2 (human): S411‑p, CtBP1 (mouse): S423‑p, CtBP1 (rat): S412‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody
 Relevant cell lines - cell types - tissues:  COS (fibroblast), NCI-H1299 (pulmonary)
 Cellular systems studied:  cell lines
 Species studied:  monkey
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE JNK1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE JNK1 (human) genetic knockout/knockin of upstream enzyme, transfection of constitutively active enzyme, activation of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
UV increase assayed phosphorylation-induced protein degradation
TNF increase assayed phosphorylation-induced protein degradation
cisplatin increase assayed phosphorylation-induced protein degradation
Downstream Regulation
 Effect of modification (function):  protein degradation
 Effect of modification (process):  apoptosis, induced
 Comments:  in H1299 cells lacking p53


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