Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 2044-5040

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice ; volume:1 ; number:1 ; day:13 ; month:10 ; year:2011 ; pages:1-13 ; date:12.2011
Skeletal muscle ; 1, Heft 1 (13.10.2011), 1-13, 12.2011

Creator: Baltgalvis, Kristen A.
Jaeger, Michele A.
Fitzsimons, Daniel P.
Thayer, Stanley A.
Lowe, Dawn A.
Ervasti, James M.

Contributor: SpringerLink (Online service)

DOI: 10.1186/2044-5040-1-32

URN: urn:nbn:de:101:1-2021083120182820077554

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:25 AM CEST

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Baltgalvis, Kristen A.
Jaeger, Michele A.
Fitzsimons, Daniel P.
Thayer, Stanley A.
Lowe, Dawn A.
Ervasti, James M.
SpringerLink (Online service)

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Mechanical factors tune the sensitivity of mdx muscle to eccentric strength loss and its protection by antioxidant and calcium modulators

Actin's role in cytokinesis and muscle contraction as studied by Cryo-Electron Tomography

Leucine-enriched essential amino acids attenuate inflammation in rat muscle and enhance muscle repair after eccentric contraction

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Functional characterization of cytoplasmic β- and γ-actin [Beta- and Gamma-actin] and cardiac actin mutations involved in cardiomyopathy

Loss of cytoplasmic actin filaments raises nuclear actin levels to drive INO80C-dependent chromosome fragmentation

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Correction to: HIF prolyl hydroxylase inhibition protects skeletal muscle from eccentric contraction induced injury

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KU-CHEN # MDX - M.XVI

Mechanical factors tune the sensitivity of mdx muscle to eccentric strength loss and its protection by antioxidant and calcium modulators

Actin's role in cytokinesis and muscle contraction as studied by Cryo-Electron Tomography

Leucine-enriched essential amino acids attenuate inflammation in rat muscle and enhance muscle repair after eccentric contraction

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Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice

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Other Objects (12)

Influence of preactivation on fascicle behavior during eccentric contraction

Actin polymerisation at the cytoplasmic face of eukaryotic nuclei

HIF prolyl hydroxylase inhibition protects skeletal muscle from eccentric contraction-induced injury

Functional characterization of cytoplasmic β- and γ-actin [Beta- and Gamma-actin] and cardiac actin mutations involved in cardiomyopathy

Loss of cytoplasmic actin filaments raises nuclear actin levels to drive INO80C-dependent chromosome fragmentation

Loss of peroxiredoxin-2 exacerbates eccentric contraction-induced force loss in dystrophin-deficient muscle

Correction to: HIF prolyl hydroxylase inhibition protects skeletal muscle from eccentric contraction induced injury

KU-CHEN # MDX - M.XVI

Mechanical factors tune the sensitivity of mdx muscle to eccentric strength loss and its protection by antioxidant and calcium modulators

Actin's role in cytokinesis and muscle contraction as studied by Cryo-Electron Tomography

Leucine-enriched essential amino acids attenuate inflammation in rat muscle and enhance muscle repair after eccentric contraction

Comparative lipidomic and metabolomic profiling of mdx and severe mdx-apolipoprotein e-null mice

Influence of preactivation on fascicle behavior during eccentric contraction

Actin polymerisation at the cytoplasmic face of eukaryotic nuclei

HIF prolyl hydroxylase inhibition protects skeletal muscle from eccentric contraction-induced injury

Functional characterization of cytoplasmic β- and γ-actin [Beta- and Gamma-actin] and cardiac actin mutations involved in cardiomyopathy

Loss of cytoplasmic actin filaments raises nuclear actin levels to drive INO80C-dependent chromosome fragmentation

Loss of peroxiredoxin-2 exacerbates eccentric contraction-induced force loss in dystrophin-deficient muscle

Correction to: HIF prolyl hydroxylase inhibition protects skeletal muscle from eccentric contraction induced injury

KU-CHEN # MDX - M.XVI

Mechanical factors tune the sensitivity of mdx muscle to eccentric strength loss and its protection by antioxidant and calcium modulators

Actin's role in cytokinesis and muscle contraction as studied by Cryo-Electron Tomography

Leucine-enriched essential amino acids attenuate inflammation in rat muscle and enhance muscle repair after eccentric contraction

Comparative lipidomic and metabolomic profiling of mdx and severe mdx-apolipoprotein e-null mice

Influence of preactivation on fascicle behavior during eccentric contraction

Actin polymerisation at the cytoplasmic face of eukaryotic nuclei

HIF prolyl hydroxylase inhibition protects skeletal muscle from eccentric contraction-induced injury

Functional characterization of cytoplasmic β- and γ-actin [Beta- and Gamma-actin] and cardiac actin mutations involved in cardiomyopathy

Loss of cytoplasmic actin filaments raises nuclear actin levels to drive INO80C-dependent chromosome fragmentation

Loss of peroxiredoxin-2 exacerbates eccentric contraction-induced force loss in dystrophin-deficient muscle

Correction to: HIF prolyl hydroxylase inhibition protects skeletal muscle from eccentric contraction induced injury

KU-CHEN # MDX - M.XVI

Mechanical factors tune the sensitivity of mdx muscle to eccentric strength loss and its protection by antioxidant and calcium modulators

Actin's role in cytokinesis and muscle contraction as studied by Cryo-Electron Tomography

Leucine-enriched essential amino acids attenuate inflammation in rat muscle and enhance muscle repair after eccentric contraction

Comparative lipidomic and metabolomic profiling of mdx and severe mdx-apolipoprotein e-null mice

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