Curated Information
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Curated Information Page
PubMed Id: 12538592 
This page summarizes selected information from the article 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.
Information from this record has been curated, but not yet edited in PhosphoSitePlus® and may be incomplete.
Yang H, et al. (2003) Phosphorylation of the Ras-GRF1 exchange factor at Ser916/898 reveals activation of Ras signaling in the cerebral cortex. J Biol Chem 278, 13278-85 12538592
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S898-p - RasGRF1 (rat)
Orthologous residues
RasGRF1 (human): S929‑p, RasGRF1 iso3 (human): S911‑p, RasGRF1 (mouse): S916‑p, RasGRF1 (rat): S898‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, mutation of modification site, phospho-antibody
 Relevant cell lines - cell types - tissues:  'neuron, cortical'-brain, COS (fibroblast), PC-12 (chromaffin)
 Cellular systems studied:  cell lines, tissue
 Species studied:  monkey, rat
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE PKACA (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE PKACA (human) pharmacological activator of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
NGF serum starvation increase
carbachol serum starvation increase
forskolin, IBMX serum starvation increase
serum serum starvation increase
thapsigargin serum starvation no change compared to control
serum starvation no change compared to control
Downstream Regulation
 Effect of modification (function):  activity, induced, intracellular localization
 Effect of modification (process):  cell growth, altered, cytoskeletal reorganization


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