Kim JE, et al. (2022) PLPP/CIN-mediated DARPP-32 serine 97 dephosphorylation delays the seizure onset in response to kainic acid in the mouse hippocampus. Neuropharmacology 219, 109238 36055413

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Y255-p - CK2A1 (mouse) ▲

Modsite: VLGTEDLyDYIDKYN SwissProt Entrez-Gene Orthologous residues CK2A1 (human): Y255‑p, CK2A1 (mouse): Y255‑p, CK2A1 (rat): Y255‑p, CK2A1 (rabbit): Y255‑p, CK2A1 (cow): Y255‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  'brain, hippocampus' Cellular systems studied:  tissue Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes PDXP (human) no change compared to control PDXP KO has no effect kainic_acid increase kainic_acid PDXP (human) augment treatment-induced increase PDXP KO inhibits

T34-p - DARPP-32 (mouse) ▲

Modsite: MIRRRRPtPAMLFRV SwissProt Entrez-Gene Orthologous residues DARPP‑32 (human): T34‑p, DARPP‑32 iso2 (human): ‑, DARPP‑32 (mouse): T34‑p, DARPP‑32 (rat): T34‑p, DARPP‑32 (cow): T34‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  'brain, hippocampus' Cellular systems studied:  tissue Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes PDXP (mouse) decrease PDXP KO increases kainic_acid increase kainic_acid PDXP (mouse) inhibit treatment-induced decrease TMCB kainic_acid inhibit treatment-induced increase TMCB kainic_acid PDXP (mouse) inhibit treatment-induced increase Downstream Regulation Effect of modification (function):  molecular association, regulation Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays PPP1CA (human) Induces co-immunoprecipitation

T75-p - DARPP-32 (mouse) ▲

Modsite: RPNPCAYtPPSLKAV SwissProt Entrez-Gene Orthologous residues DARPP‑32 (human): T75‑p, DARPP‑32 iso2 (human): T39‑p, DARPP‑32 (mouse): T75‑p, DARPP‑32 (rat): T75‑p, DARPP‑32 (cow): T75‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  'brain, hippocampus' Cellular systems studied:  tissue Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes PDXP (human) no change compared to control PLPP KO has no effect kainic_acid increase kainic_acid PDXP (mouse) no effect upon treatment-induced increase PDXP KO has no effect

S97-p - DARPP-32 (mouse) ▲

Modsite: NLsENQAsEEEDELG SwissProt Entrez-Gene Orthologous residues DARPP‑32 (human): S102‑p, DARPP‑32 iso2 (human): S66‑p, DARPP‑32 (mouse): S97‑p, DARPP‑32 (rat): S102‑p, DARPP‑32 (cow): S102‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  'brain, hippocampus' Cellular systems studied:  tissue Species studied:  mouse Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes PHOSPHATASE PDXP (human) co-immunoprecipitation, genetic knockout/knockin of upstream enzyme KINASE CK2A1 (mouse) pharmacological inhibitor of upstream enzyme, phospho-antibody Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes PDXP (mouse) decrease PDXP KO increases kainic_acid increase kainic_acid PDXP (mouse) inhibit treatment-induced decrease TMCB kainic_acid inhibit treatment-induced increase TMCB kainic_acid PDXP (mouse) inhibit treatment-induced increase TMCB decrease Downstream Regulation Effect of modification (function):  molecular association, regulation, phosphorylation Effect of modification (process):  signaling pathway regulation Modification regulates interactions with:  Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays PPP1CA (human) Induces co-immunoprecipitation Comments:  inhibits GluR1 dephosphorylation, thus inducing DARPP-32-PP1-GRIA1 signaling

S863-p - GluR1 (mouse) ▲

Modsite: tstLPRNsGAGASGG SwissProt Entrez-Gene Orthologous residues GluR1 (human): S863‑p, GluR1 iso6 (human): S873‑p, GluR1 (mouse): S863‑p, GluR1 (rat): S863‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  'brain, hippocampus' Cellular systems studied:  tissue Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes PDXP (human) no change compared to control PDXP KO has no effect kainic_acid increase kainic_acid PDXP (human) augment treatment-induced increase PDXP KO inhibits TMCB kainic_acid inhibit treatment-induced increase TMCB PDXP (human) inhibit treatment-induced increase

T198-p - PKACA (mouse) ▲

Modsite: RVKGRtWtLCGtPEY SwissProt Entrez-Gene Orthologous residues PKACA (human): T198‑p, PKACA iso2 (human): T191‑p, PKACA (mouse): T198‑p, PKACA (rat): T198‑p, PKACA (pig): T198‑p, PKACA (dog): T197‑p, PKACA (cow): T198‑p Characterization Methods used to characterize site in vivo:  phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  'brain, hippocampus' Cellular systems studied:  tissue Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes PDXP (human) no change compared to control PDXP KO has no effect kainic_acid increase kainic_acid PDXP (human) augment treatment-induced increase PDXP KO inhibits TMCB kainic_acid inhibit treatment-induced increase TMCB PDXP (human) inhibit treatment-induced increase