Curated Information
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Home > Curated Information Page > PubMed Id: 17178402
Kim WY, et al. (2006) Essential roles for GSK-3s and GSK-3-primed substrates in neurotrophin-induced and hippocampal axon growth. Neuron 52, 981-96 17178402
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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Y504-p - CRMP-1 (mouse)
Modsite: GMyDGPVyEVPAtPk SwissProt Entrez-Gene
Orthologous residues
CRMP‑1 (human): Y504‑p, CRMP‑1 iso2 (human): Y618‑p, CRMP‑1 (mouse): Y504‑p, CRMP‑1 iso2 (mouse): Y425‑p, CRMP‑1 (rat): Y504‑p
Characterization
Methods used to characterize site in vivo microscopy-colocalization with upstream kinase, western blotting
Relevant cell lines - cell types - tissues:  neuron-'brain, hippocampus' [GSK3B (mouse)]
Cellular systems studied:  primary cultured cells
Species studied:  mouse
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
decrease GSK-3 KM Mutant (kinase dead); GSK-3 R96A mutant (axon branching defect)
GSK-3_inhibitor_X decrease

T509-p - CRMP-1 (mouse)
Modsite: PVyEVPAtPkHAAPA SwissProt Entrez-Gene
Orthologous residues
CRMP‑1 (human): T509‑p, CRMP‑1 iso2 (human): T623‑p, CRMP‑1 (mouse): T509‑p, CRMP‑1 iso2 (mouse): T430‑p, CRMP‑1 (rat): T509‑p
Characterization
Methods used to characterize site in vivo microscopy-colocalization with upstream kinase, western blotting
Relevant cell lines - cell types - tissues:  neuron-'brain, hippocampus' [GSK3B (mouse)]
Cellular systems studied:  primary cultured cells
Species studied:  mouse
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
decrease GSK-3 KM Mutant (kinase dead); GSK-3 R96A mutant (axon branching defect)
GSK-3_inhibitor_X decrease

S9-p - GSK3B (mouse)
Modsite: SGRPRttsFAEsCKP SwissProt Entrez-Gene
Orthologous residues
GSK3B (human): S9‑p, GSK3B iso2 (human): S9‑p, GSK3B (mouse): S9‑p, GSK3B (rat): S9‑p, GSK3B (rabbit): S9‑p
Characterization
Methods used to characterize site in vivo microscopy-colocalization with upstream kinase, western blotting
Relevant cell lines - cell types - tissues:  neuron-'brain, hippocampus' [GSK3B (mouse)]
Cellular systems studied:  primary cultured cells
Species studied:  mouse

S1260-p - MAP1B (mouse)
Modsite: sLsPsPPsPIEKtPL SwissProt Entrez-Gene
Orthologous residues
MAP1B (human): S1265‑p, MAP1B (mouse): S1260‑p, MAP1B (rat): S1256‑p, MAP1B (cow): S1259‑p
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
no change compared to control GSK-3 R96A mutant (axon branching defect
decrease GSK-3 KM Mutant (kinase dead)
decrease GSK-3 KM Mutant (kinase dead); GSK-3 R96A mutant (axon branching defect
GSK-3_inhibitor_X decrease

T1265-p - MAP1B (mouse)
Modsite: PPsPIEKtPLGERsV SwissProt Entrez-Gene
Orthologous residues
MAP1B (human): T1270‑p, MAP1B (mouse): T1265‑p, MAP1B (rat): T1261‑p, MAP1B (cow): T1264‑p
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
no change compared to control GSK-3 R96A mutant (axon branching defect
decrease GSK-3 KM Mutant (kinase dead)
decrease GSK-3 KM Mutant (kinase dead); GSK-3 R96A mutant (axon branching defect
GSK-3_inhibitor_X decrease