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November 18, 2005Proceedings of the National Academy of SciencesOpen Access

Myosin light chain kinase and myosin phosphorylation effect frequency-dependent potentiation of skeletal muscle contraction

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Population

MYLK2 knockout mice and wild-type mice

Comparison

Ablation of the MYLK2 gene… vs Wild-type mice

Design

Preclinical

Key result

Ablation of the MYLK2 gene in mice attenuated posttetanic and low-frequency twitch-tension potentiation in fast-twitch skeletal muscles.

Authors

GZGang ZhiJRJeffrey W. RyderJHJian Huang

Discussion

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Overview

MLCK confirmed as key mediator of potentiation in mice; leaves open translation to human muscle function or disease.

Structured PICO

P
Population
MYLK2 knockout mice and wild-type mice
I
Intervention
Ablation of the MYLK2 gene (Ca(2+)/calmodulin-dependent skeletal muscle myosin light chain kinase)
C
Comparator
Wild-type mice
O
Outcome
Myosin regulatory light chain (RLC) phosphorylation and isometric twitch-tension potentiation in response to repetitive electrical stimulationsurrogate

Myosin light chain phosphorylation by skeletal muscle MLCK is a primary biochemical mechanism for tension potentiation due to repetitive stimulation in fast-twitch skeletal muscle.

Cite This Study

Zhi et al. (2005) studied Skeletal muscle contraction. Ablation of the MYLK2 gene (MLCK knockout) vs. Wild-type mice was evaluated on RLC phosphorylation and isometric twitch-tension potentiation. Ablation of the MYLK2 gene in mice attenuated posttetanic and low-frequency twitch-tension potentiation in fast-twitch skeletal muscles.

synapsesocial.com/papers/6a22703bf4540fbb2453e8b1https://doi.org/10.1073/pnas.0506846102
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