Curated Information
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Home > Curated Information Page > PubMed Id: 18460467
Cole AR, et al. (2008) Relative Resistance of Cdk5-phosphorylated CRMP2 to Dephosphorylation. J Biol Chem 283, 18227-18237 18460467
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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T509-p - CRMP-2 (rat)
Modsite: PVCEVSVtPKTVtPA SwissProt Entrez-Gene
Orthologous residues
CRMP‑2 (human): T509‑p, CRMP‑2 iso3 (human): T614‑p, CRMP‑2 (mouse): T509‑p, CRMP‑2 (rat): T509‑p, CRMP‑2 (chicken): T509‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  neuroblastoma
Relevant cell lines - cell types - tissues:  'neuron, cortical', 293 (epithelial), SH-SY5Y (neural crest)
Cellular systems studied:  cell lines, primary cells
Species studied:  human, rat
Enzymes shown to modify site in vitro
Type Enzyme
PHOSPHATASE PPP1CA (human)
KINASE GSK3B (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE GSK3B (human) pharmacological inhibitor of upstream enzyme, genetic transfer of constitutively active upstream enzyme, phospho-antibody
PHOSPHATASE PPP1CA (human) pharmacological inhibitor of upstream enzyme, phospho-antibody
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
okadaic_acid increase
calyculin_A increase
cypermethrin no change compared to control
ciclosporin no change compared to control
CT-99021 decrease
calyculin_A CT-99021 inhibit treatment-induced decrease
IGF-1 decrease
calyculin_A IGF-1 inhibit treatment-induced decrease
okadaic_acid IGF-1 inhibit treatment-induced decrease
IGF-1 GSK3B (mouse) inhibit treatment-induced decrease
EGTA no change compared to control
BAPTA-AM no change compared to control
purvalanol decrease
alsterpaullone decrease
PIN1 (human) no change compared to control

T514-p - CRMP-2 (rat)
Modsite: SVtPKTVtPASsAKT SwissProt Entrez-Gene
Orthologous residues
CRMP‑2 (human): T514‑p, CRMP‑2 iso3 (human): T619‑p, CRMP‑2 (mouse): T514‑p, CRMP‑2 (rat): T514‑p, CRMP‑2 (chicken): T514‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  neuroblastoma
Relevant cell lines - cell types - tissues:  'neuron, cortical', 293 (epithelial), SH-SY5Y (neural crest)
Cellular systems studied:  cell lines, primary cells
Species studied:  human, rat
Enzymes shown to modify site in vitro
Type Enzyme
PHOSPHATASE PPP1CA (human)
KINASE GSK3B (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE GSK3B (human) pharmacological inhibitor of upstream enzyme, genetic transfer of constitutively active upstream enzyme, phospho-antibody
PHOSPHATASE PPP1CA (human) pharmacological inhibitor of upstream enzyme, phospho-antibody
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
okadaic_acid increase
calyculin_A increase
cypermethrin no change compared to control
ciclosporin no change compared to control
CT-99021 decrease
calyculin_A CT-99021 inhibit treatment-induced decrease
IGF-1 decrease
calyculin_A IGF-1 inhibit treatment-induced decrease
okadaic_acid IGF-1 inhibit treatment-induced decrease
IGF-1 GSK3B (mouse) inhibit treatment-induced decrease
EGTA no change compared to control
BAPTA-AM no change compared to control
purvalanol decrease
alsterpaullone decrease
PIN1 (human) no change compared to control

S522-p - CRMP-2 (rat)
Modsite: PASsAKTsPAKQQAP SwissProt Entrez-Gene
Orthologous residues
CRMP‑2 (human): S522‑p, CRMP‑2 iso3 (human): S627‑p, CRMP‑2 (mouse): S522‑p, CRMP‑2 (rat): S522‑p, CRMP‑2 (chicken): S522‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  neuroblastoma
Relevant cell lines - cell types - tissues:  'neuron, cortical', 293 (epithelial), SH-SY5Y (neural crest)
Cellular systems studied:  cell lines, primary cells
Species studied:  human, rat
Enzymes shown to modify site in vitro
Type Enzyme
KINASE CDK5 (human)
PHOSPHATASE PPP1CA (human)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK5 (human) pharmacological inhibitor of upstream enzyme, phospho-antibody
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
IGF-1 no change compared to control
EGTA no change compared to control
BAPTA-AM no change compared to control
okadaic_acid no change compared to control
calyculin_A no change compared to control
cypermethrin no change compared to control
ciclosporin no change compared to control
purvalanol decrease
CT-99021 no change compared to control
alsterpaullone no change compared to control
PIN1 (human) no change compared to control

S522-p - CRMP-4 (rat)
Modsite: PAGsTRGsPTRPNPP SwissProt Entrez-Gene
Orthologous residues
CRMP‑4 (human): S522‑p, CRMP‑4 iso2 (human): S636‑p, CRMP‑4 (mouse): S522‑p, CRMP‑4 iso3 (mouse): , CRMP‑4 (rat): S522‑p, CRMP‑4 iso2 (rat): S635‑p, CRMP‑4 (cow): S636‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Disease tissue studied:  neuroblastoma
Relevant cell lines - cell types - tissues:  'neuron, cortical', 293 (epithelial), SH-SY5Y (neural crest)
Cellular systems studied:  cell lines, primary cells
Species studied:  human, rat