Begum G, et al. (2015) Inhibition of WNK3 Kinase Signaling Reduces Brain Damage and Accelerates Neurological Recovery After Stroke. Stroke 46, 1956-65 26069258

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.

Click on the protein name to open the protein page, and on the RSD number to open the site page.

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T196-p - NKCC1 (mouse) ▲

Modsite: HQQYYYDtHTNtYYL SwissProt Entrez-Gene Orthologous residues NKCC1 (human): T203‑p, NKCC1 iso3 (human): T203‑p, NKCC1 (mouse): T196‑p, NKCC1 (rat): T194‑p Characterization Methods used to characterize site in vivo:  immunoassay, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  neuron, oligodendrocyte Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ischemia/reperfusion increase ischemia/reperfusion WNK3 (mouse) augment treatment-induced increase Downstream Regulation Effect of modification (function):  enzymatic activity, induced Comments:  Ischemic cell death Associated Diseases Diseases Alterations Comments stroke, ischemia increased

T200-p - NKCC1 (mouse) ▲

Modsite: YYDtHTNtYYLRtFG SwissProt Entrez-Gene Orthologous residues NKCC1 (human): T207‑p, NKCC1 iso3 (human): T207‑p, NKCC1 (mouse): T200‑p, NKCC1 (rat): T198‑p Characterization Methods used to characterize site in vivo:  immunoassay, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  neuron, oligodendrocyte Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ischemia/reperfusion increase ischemia/reperfusion WNK3 (mouse) augment treatment-induced increase Downstream Regulation Effect of modification (function):  enzymatic activity, induced Comments:  Ischemic cell death Associated Diseases Diseases Alterations Comments stroke, ischemia increased

T205-p - NKCC1 (mouse) ▲

Modsite: TNtYYLRtFGHNtMD SwissProt Entrez-Gene Orthologous residues NKCC1 (human): T212‑p, NKCC1 iso3 (human): T212‑p, NKCC1 (mouse): T205‑p, NKCC1 (rat): T203‑p Characterization Methods used to characterize site in vivo:  immunoassay, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  neuron, oligodendrocyte Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ischemia/reperfusion increase ischemia/reperfusion WNK3 (mouse) augment treatment-induced increase Downstream Regulation Effect of modification (function):  enzymatic activity, induced Comments:  Ischemic cell death Associated Diseases Diseases Alterations Comments stroke, ischemia increased

T185-p - OSR1 (mouse) ▲

Modsite: TRNKVRKtFVGtPCW SwissProt Entrez-Gene Orthologous residues OSR1 (human): T185‑p, OSR1 (mouse): T185‑p, OSR1 (rat): T185‑p Characterization Methods used to characterize site in vivo:  immunoassay, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  neuron, oligodendrocyte Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ischemia/reperfusion increase ischemia/reperfusion WNK3 (mouse) augment treatment-induced increase hypoxia/reoxygenation increase hypoxia/reoxygenation WNK3 (mouse) no effect upon treatment-induced increase WNK3 siRNA decrease Associated Diseases Diseases Alterations Comments stroke, ischemia increased

T236-p - STLK3 (mouse) ▲

Modsite: LATGGDVtRNKVRKt SwissProt Entrez-Gene Orthologous residues STLK3 (human): T224‑p, STLK3 (mouse): T236‑p, STLK3 (rat): T233‑p Characterization Methods used to characterize site in vivo:  immunoassay, phospho-antibody, western blotting Relevant cell lines - cell types - tissues:  neuron, oligodendrocyte Cellular systems studied:  primary cells Species studied:  mouse Upstream Regulation Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes ischemia/reperfusion increase ischemia/reperfusion WNK3 (mouse) augment treatment-induced increase hypoxia/reoxygenation increase hypoxia/reoxygenation WNK3 (mouse) no effect upon treatment-induced increase WNK3 siRNA decrease Associated Diseases Diseases Alterations Comments stroke, ischemia increased