PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice

PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice

Jingliang Zhang et al. examine how dysfunctional PKA signaling impacts neuronal activity and seizure susceptibility in a mouse model of temporal lobe epilepsy. Their data suggest that autophosphorylation of the RIIβ subunit regulates neuronal excitability, and may act as a future therapeutic target....

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Main Authors: Jingliang Zhang, Chenyu Zhang, Xiaoling Chen, Bingwei Wang, Weining Ma, Yang Yang, Ruimao Zheng, Zhuo Huang
Format: Article
Language:English
Published: Nature Publishing Group 2021-03-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-021-01748-4
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spelling doaj-9c4c3b9f0dd34dfd9978b39e043e5a312021-03-11T12:03:53ZengNature Publishing GroupCommunications Biology2399-36422021-03-014111410.1038/s42003-021-01748-4PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in miceJingliang Zhang0Chenyu Zhang1Xiaoling Chen2Bingwei Wang3Weining Ma4Yang Yang5Ruimao Zheng6Zhuo Huang7State Key Laboratory of Natural and Biomimetic Drugs, Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University Health Science CenterDepartment of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University Health Science CenterState Key Laboratory of Natural and Biomimetic Drugs, Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University Health Science CenterDepartment of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University Health Science CenterDepartment of Neurology, Shengjing Hospital Affiliated to China Medical UniversityDepartment of Medicinal Chemistry and Molecular Pharmacology, Purdue University College of PharmacyDepartment of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University Health Science CenterState Key Laboratory of Natural and Biomimetic Drugs, Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University Health Science CenterJingliang Zhang et al. examine how dysfunctional PKA signaling impacts neuronal activity and seizure susceptibility in a mouse model of temporal lobe epilepsy. Their data suggest that autophosphorylation of the RIIβ subunit regulates neuronal excitability, and may act as a future therapeutic target.https://doi.org/10.1038/s42003-021-01748-4
collection DOAJ
language English
format Article
sources DOAJ
author Jingliang Zhang
Chenyu Zhang
Xiaoling Chen
Bingwei Wang
Weining Ma
Yang Yang
Ruimao Zheng
Zhuo Huang
spellingShingle Jingliang Zhang
Chenyu Zhang
Xiaoling Chen
Bingwei Wang
Weining Ma
Yang Yang
Ruimao Zheng
Zhuo Huang
PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice
Communications Biology
author_facet Jingliang Zhang
Chenyu Zhang
Xiaoling Chen
Bingwei Wang
Weining Ma
Yang Yang
Ruimao Zheng
Zhuo Huang
author_sort Jingliang Zhang
title PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice
title_short PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice
title_full PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice
title_fullStr PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice
title_full_unstemmed PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice
title_sort pka-riiβ autophosphorylation modulates pka activity and seizure phenotypes in mice
publisher Nature Publishing Group
series Communications Biology
issn 2399-3642
publishDate 2021-03-01
description Jingliang Zhang et al. examine how dysfunctional PKA signaling impacts neuronal activity and seizure susceptibility in a mouse model of temporal lobe epilepsy. Their data suggest that autophosphorylation of the RIIβ subunit regulates neuronal excitability, and may act as a future therapeutic target.
url https://doi.org/10.1038/s42003-021-01748-4
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