Curated Information
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Curated Information Page
PubMed Id: 15241487 
Domina AM, et al. (2004) MCL1 is phosphorylated in the PEST region and stabilized upon ERK activation in viable cells, and at additional sites with cytotoxic okadaic acid or taxol. Oncogene 23, 5301-15 15241487
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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T163-p - MCL1 (human)
Orthologous residues
MCL1 (human): T163‑p, MCL1 iso2 (human): T163‑p, MCL1 (mouse): T144‑p, MCL1 (rat): T143‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Disease tissue studied:  lymphoma, Burkitt's lymphoma
 Relevant cell lines - cell types - tissues:  BL-41 (B lymphocyte), CHO (fibroblast) [EphB1 (human), transfection]
 Cellular systems studied:  cell lines
 Species studied:  hamster, human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE ERK2 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE ERK2 (human) pharmacological inhibitor of upstream enzyme, pharmacological activator of upstream enzyme
KINASE ERK1 (human) pharmacological inhibitor of upstream enzyme, pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
phorbol ester increase
U0126 phorbol ester inhibit treatment-induced increase
okadaic acid no change compared to control
taxol no change compared to control


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