Curated Information
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Curated Information Page
PubMed Id: 12818177 
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.
Wang Q, et al. (2003) Control of synaptic strength, a novel function of Akt. Neuron 38, 915-28 12818177
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S434-p - GABRB2 (rat)
Orthologous residues
GABRB2 (human): S472‑p, GABRB2 iso1 (human): S434‑p, GABRB2 (mouse): S472‑p, GABRB2 iso2 (mouse): S434‑p, GABRB2 (rat): S434‑p
Characterization
 Methods used to characterize site in vivo [32P] bio-synthetic labeling, mutation of modification site
 Relevant cell lines - cell types - tissues:  'neuron, hippocampal'-brain, 293 (epithelial)
 Cellular systems studied:  cell lines, primary cultured cells
 Species studied:  human, rat
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE Akt1 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE Akt1 (human) transfection of wild-type enzyme, transfection of inactive enzyme, genetic transfer of inducible upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
LY294002 insulin inhibit treatment-induced increase
8-Rp-cAMP insulin no effect upon treatment-induced increase
Go 6850 insulin no effect upon treatment-induced increase
LY294002 decrease
Downstream Regulation
 Effect of modification (function):  intracellular localization


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