CaMKIIβ Signaling drives expression of metabolic and stress response genes in skeletal muscle, and its loss contributes to the LGMDR1 phenotype.

doi:10.1093/hmg/ddag090

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Article

CaMKIIβ Signaling drives expression of metabolic and stress response genes in skeletal muscle, and its loss contributes to the LGMDR1 phenotype.

Human molecular genetics - 11 Sept 2026

Kramerova Irina, Anastopulos Frieda, Becerra Diana, Goldstein de Salazar Ruby, Keeble Alexander R, Chamberlain Jeffrey S, Moore Steven A, McNally Elizabeth M, Spencer Melissa J

Abstract excerpt

Calcium calmodulin kinase II (CaMKII) signaling is activated by muscle use and drives gene expression that promotes slow oxidative muscle phenotype. Previously, we showed that the calpain 3 knockout (C3KO) mouse model of limb girdle muscular dystrophy R1 (LGMDR1) exhibits impaired slow-oxidative gene expression and these deficits were associated with reduced levels of the CaMKIIβ isoform and attenuated CaMKII...

Read the complete abstract on PubMed

Topics

Animals
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Muscle, Skeletal
Mice
Muscular Dystrophies, Limb-Girdle

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Signal Transduction

Mice, Knockout

Humans

Calpain

Disease Models, Animal

Phenotype

Gene Expression Regulation

Oxidative Stress

Muscle Proteins

Source

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Identifiers

PMID: 42725915
DOI: 10.1093/hmg/ddag090
PMCID: PMC13626206

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