Protein Kinase A in neurological disorders

被引：6

作者：

Glebov-McCloud, Alexander G. P. ^{[1
]}

Saide, Walter S. ^{[1
]}

Gaine, Marie E. ^{[2
,3
]}

Strack, Stefan ^{[1
,3
]}

机构：

[1] Univ Iowa, Carver Coll Med, Dept Neurosci & Pharmacol, Bowen Sci Bldg 51 Newton Rd, Iowa City, IA 52242 USA

[2] Univ Iowa, Coll Pharm Bldg, Dept Pharmaceut Sci & Expt Therapeut, 180 S Grand Ave, Iowa City, IA 52242 USA

[3] Iowa Neurosci Inst, Intellectual & Dev Disabil Res Ctr, Iowa City, IA 52242 USA

来源：

JOURNAL OF NEURODEVELOPMENTAL DISORDERS | 2024年 / 16卷 / 01期

关键词：

PKA; cAMP; Protein phosphorylation; CREB; Gene transcription; MAPK; Kinases; Neurodevelopment; Learning; Memory; Cognition; Endocrine Systems; Metabolic Disorders; Movement Disorders; Neurodegeneration; SIGNAL-REGULATED KINASE; CATALYTIC SUBUNIT; MOLECULAR-CLONING; RABBIT SKELETAL; SPLICE VARIANTS; RI-ALPHA; IN-VIVO; C-BETA; SOMATIC MUTATIONS; AKAP SPECIFICITY;

D O I：

10.1186/s11689-024-09525-0

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Cyclic adenosine 3', 5' monophosphate (cAMP)-dependent Protein Kinase A (PKA) is a multi-functional serine/threonine kinase that regulates a wide variety of physiological processes including gene transcription, metabolism, and synaptic plasticity. Genomic sequencing studies have identified both germline and somatic variants of the catalytic and regulatory subunits of PKA in patients with metabolic and neurodevelopmental disorders. In this review we discuss the classical cAMP/PKA signaling pathway and the disease phenotypes that result from PKA variants. This review highlights distinct isoform-specific cognitive deficits that occur in both PKA catalytic and regulatory subunits, and how tissue-specific distribution of these isoforms may contribute to neurodevelopmental disorders in comparison to more generalized endocrine dysfunction.

引用

页数：11

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