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Orthologous residues
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RKIP (human): S153‑p, RKIP (mouse): T153‑p, RKIP (rat): S153‑p
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Characterization
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Methods used to characterize site in vivo:
mutation of modification site, phospho-antibody
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Relevant cell lines - cell types - tissues:
H19-7 (neuron) [IGF1R (human)]
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Cellular systems studied:
cell lines
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Species studied:
rat
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Enzymes shown to modify site in vitro:
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Comments:
Classic and atypical but not novel PKC isoforms phosphorylate RKIP at serine 153.
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Upstream Regulation
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Potential in vivo enzymes for site:
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Type
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Enzyme
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Evidence
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Notes
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KINASE
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PKCA (rat)
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pharmacological activator of upstream enzyme, pharmacological inhibitor of upstream enzyme
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Although the exact PKC isotype(s) responsible for in vivo phosphorylation were not proven in this paper, in vitro evidence indicates that classic and atypical but not novel PKC isoforms phosphorylate RKIP at serine 153.
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Treatments, proteins and their effect on site modification:
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Treatments
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Referenced Treatments
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Manipulated Protein
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Referenced Protein
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Effect
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Notes
|
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phorbol ester
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|
|
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increase
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|
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EGF
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|
|
|
increase
|
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|
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Downstream Regulation
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Effect of modification (function):
molecular association, regulation
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Modification regulates interactions with:
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|
Interacting molecule
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Interacting domains
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Effect
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Consequences (function)
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Consequences (process)
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Detection assays
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c-Raf (rat)
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Disrupts
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enzymatic activity, inhibited
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|
co-immunoprecipitation
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|
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Comments:
RKIP inhibits MAP kinase activation in response to growth factors or PKC activators, and PKC can regulate Raf-1 signaling through phosphorylation of RKIP. Classical and atypical PKCs phosphorylate RKIP on Ser-153, which results in the displacement of RKIP from Raf-1, freeing Raf-1 to activate downstream targets..
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