Curated Information
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Curated Information Page
PubMed Id: 15664178 
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.
Tomita S, et al. (2005) Bidirectional synaptic plasticity regulated by phosphorylation of stargazin-like TARPs. Neuron 45, 269-77 15664178
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
Download Sites

S228-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S228‑p, CACNG2 (mouse): S228‑p, CACNG2 (rat): S228‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation

S237-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S237‑p, CACNG2 (mouse): S237‑p, CACNG2 (rat): S237‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation

S239-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S239‑p, CACNG2 (mouse): S239‑p, CACNG2 (rat): S239‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation

S240-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S240‑p, CACNG2 (mouse): S240‑p, CACNG2 (rat): S240‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation

S241-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S241‑p, CACNG2 (mouse): S241‑p, CACNG2 (rat): S241‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation

S243-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S243‑p, CACNG2 (mouse): S243‑p, CACNG2 (rat): S243‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation

S247-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S247‑p, CACNG2 (mouse): S247‑p, CACNG2 (rat): S247‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation

S249-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S249‑p, CACNG2 (mouse): S249‑p, CACNG2 (rat): S249‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation

S253-p - CACNG2 (mouse) ▲
Orthologous residues
CACNG2 (human): S253‑p, CACNG2 (mouse): S253‑p, CACNG2 (rat): S253‑p
Characterization
 Methods used to characterize site in vivo:  2D analysis, [32P] bio-synthetic labeling, electrophoretic mobility shift, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
 Relevant cell lines - cell types - tissues:  'brain, hippocampus', CHO (fibroblast), neuron-'brain, cerebral cortex', oocyte
 Cellular systems studied:  cell lines, primary cells, primary cultured cells, tissue
 Species studied:  frog, hamster, mouse
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
TTX increase
APV increase
tautomycin increase
okadaic acid increase
FK506 increase
NMDA decrease
KN-93 NMDA augment treatment-induced decrease inhibits the recovery
GF109203X NMDA augment treatment-induced decrease inhibits the recovery
PD98059 NMDA no effect upon treatment-induced decrease
KT5720 NMDA no effect upon treatment-induced decrease
Downstream Regulation
 Effect of modification (function):  activation
 Comments:  enhances AMPA receptor responses and is required for long-term potentiation


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