Publication: ERK1/2-Dependent Phosphorylation of GABA${B1}$(S867/T872), Controlled by CaMKIIβ, Is Required for GABA${B}$ Receptor Degradation under Physiological and Pathological Conditions
ERK1/2-Dependent Phosphorylation of GABA${B1}$(S867/T872), Controlled by CaMKIIβ, Is Required for GABA${B}$ Receptor Degradation under Physiological and Pathological Conditions
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Bhat, M. A., Grampp, T., & Benke, D. (2023). ERK1/2-Dependent Phosphorylation of GABA${B1}$(S867/T872), Controlled by CaMKIIβ, Is Required for GABA${B}$ Receptor Degradation under Physiological and Pathological Conditions. International Journal of Molecular Sciences, 24(17), 13436. https://doi.org/10.3390/ijms241713436
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GABA${B}$ receptor-mediated inhibition is indispensable for maintaining a healthy neuronal excitation/inhibition balance. Many neurological diseases are associated with a disturbed excitation/inhibition balance and downregulation of GABA${B}$ receptors due to enhanced sorting of the receptors to lysosomal degradation. A key event triggering the downregulation of the receptors is the phosphorylation of S867 in the GABA${B1}$ subunit mediated by CaMKIIβ. Interestingly, close to S867 in GABA${B1}$
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Bhat, M. A., Grampp, T., & Benke, D. (2023). ERK1/2-Dependent Phosphorylation of GABA${B1}$(S867/T872), Controlled by CaMKIIβ, Is Required for GABA${B}$ Receptor Degradation under Physiological and Pathological Conditions. International Journal of Molecular Sciences, 24(17), 13436. https://doi.org/10.3390/ijms241713436