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Orthologous residues
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|
PAR‑4 (human): T163‑p, PAR‑4 (mouse): T156‑p, PAR‑4 (rat): T155‑p
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Characterization
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Methods used to characterize site in vivo:
[32P] bio-synthetic labeling, mutation of modification site, phospho-antibody, western blotting
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Disease tissue studied:
breast cancer, leukemia, erythroid leukemia, lung cancer, non-small cell lung cancer, prostate cancer
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Relevant cell lines - cell types - tissues:
3T3 (fibroblast), A549 (pulmonary), HEL (erythroid), LNCaP (prostate cell), lung, MCF-10A (breast cell), MCF-7 (breast cell), MD435 (breast cell), MDA-MB231 (breast cell), MEF (fibroblast), NCI-H157 (pulmonary), NCI-H460 (pulmonary), NCI-H838 (pulmonary), PC3 (prostate cell)
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Cellular systems studied:
cell lines, primary cells
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Species studied:
human, mouse
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Enzymes shown to modify site in vitro:
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|
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Upstream Regulation
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|
Potential in vivo enzymes for site:
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|
Type
|
Enzyme
|
Evidence
|
Notes
|
|
KINASE
|
PKACa (human)
|
modification site within consensus motif, pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme, phospho-antibody, transfection of wild-type enzyme
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|
|
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Treatments, proteins and their effect on site modification:
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|
Treatments
|
Referenced Treatments
|
Manipulated Protein
|
Referenced Protein
|
Effect
|
Notes
|
|
cAMP analog
|
|
|
|
increase
|
|
|
mPKI
|
cAMP analog
|
|
|
inhibit treatment-induced increase
|
|
|
mPKI
|
|
|
|
decrease
|
|
|
vincristine
|
|
|
|
increase
|
|
|
|
Downstream Regulation
|
|
Effect of modification (process):
apoptosis, induced, transcription, altered
|
|
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