Key result
Tmod1 deletion caused Tmod3 mislocalization and destabilization of the Tmod3-γ(cyto)-actin-sAnk1.5 complex, leading to SR morphological defects, impaired Ca(2+) release, and sarcomere misalignment.
Population
Skeletal muscle fibers
Comparison
Tmod1 deletion (genetic targeting approach) vs Wild-type muscle fibers
Design
Preclinical
Authors
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Tmod3-sAnk1.5 axis stabilizes SR in mice; leaves open relevance to human Ca2+ disorders or cardiomyopathy.
Tmod3 regulates SR-associated γ(cyto)-actin architecture and mechanically stabilizes the SR via a novel cytoskeletal linkage to sAnk1.5, maintaining alignment of adjacent myofibrils.
Gokhin et al. (2011) studied this question. Tmod1 deletion vs. Wild-type muscle fibers was evaluated on Organization of cytoplasmic γ-actin in the sarcoplasmic reticulum. Tmod1 deletion caused Tmod3 mislocalization and destabilization of the Tmod3-γ(cyto)-actin-sAnk1.5 complex, leading to SR morphological defects, impaired Ca(2+) release, and sarcomere misalignment.
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