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Titin, a Central Mediator for Hypertrophic Signaling, Exercise-Induced Mechanosignaling and Skeletal Muscle Remodeling.
- Published in:
- Frontiers in Physiology, 2016, p. 1, doi. 10.3389/fphys.2016.00076
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- Article
Acute exercise modifies titin phosphorylation and increases cardiac myofilament stiffness.
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- Frontiers in Physiology, 2014, v. 5, p. 1, doi. 10.3389/fphys.2014.00449
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- Article
Systematic Analysis Reveals Elongation Factor 2 and α-Enolase as Novel Interaction Partners of AKT2.
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- PLoS ONE, 2013, v. 8, n. 6, p. 1, doi. 10.1371/journal.pone.0066045
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- Article
Protein Quality Control at the Sarcomere: Titin Protection and Turnover and Implications for Disease Development.
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- Frontiers in Physiology, 2022, v. 13, p. 1, doi. 10.3389/fphys.2022.914296
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- Article
E3-ligase knock down revealed differential titin degradation by autopagy and the ubiquitin proteasome system.
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- Scientific Reports, 2021, v. 11, n. 1, p. 1, doi. 10.1038/s41598-021-00618-7
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- Article
Titin: central player of hypertrophic signaling and sarcomeric protein quality control.
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- Biological Chemistry, 2014, v. 395, n. 11, p. 1341, doi. 10.1515/hsz-2014-0178
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- Article
Differential changes in titin domain phosphorylation increase myofilament stiffness in failing human hearts.
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- Cardiovascular Research, 2013, v. 99, n. 4, p. 648
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- Article
Molecular and cellular evidence for the impact of a hypertrophic cardiomyopathy-associated RAF1 variant on the structure and function of contractile machinery in bioartificial cardiac tissues.
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- Communications Biology, 2023, v. 6, n. 1, p. 1, doi. 10.1038/s42003-023-05013-8
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- Article