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Marta Canato

Researcher at University of Padua

Publications -  39
Citations -  1485

Marta Canato is an academic researcher from University of Padua. The author has contributed to research in topics: Calsequestrin & Skeletal muscle. The author has an hindex of 18, co-authored 36 publications receiving 1243 citations. Previous affiliations of Marta Canato include University of Rochester Medical Center.

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DRP1-mediated mitochondrial shape controls calcium homeostasis and muscle mass

TL;DR: It is shown that genetic ablation of the pro-fission protein DRP1 leads to accumulation of abnormal mitochondria that induce muscle atrophy by altering Ca2+ homeostasis and cellular stress responses.
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Inducible activation of Akt increases skeletal muscle mass and force without satellite cell activation

TL;DR: An inducible transgenic model of muscle hypertrophy by short‐term Akt activation by showing that during a fast hyper‐trophic growth myonuclear domain can increase without compromising muscle performance can be concluded.
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Reorganized stores and impaired calcium handling in skeletal muscle of mice lacking calsequestrin-1

TL;DR: Results demonstrate that CS1 is essential for the normal development of the SR and its calcium release units and for the storage and release of appropriate amounts of SR Ca2+.
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Anesthetic- and heat-induced sudden death in calsequestrin-1-knockout mice

TL;DR: In vitro studies indicate that CASQ1‐null muscle exhibits increased contractile sensitivity to temperature and caffeine, temperature‐dependent increases in resting Ca2+, and an increase in the magnitude of depolarization‐induced Ca2+ release.
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Massive alterations of sarcoplasmic reticulum free calcium in skeletal muscle fibers lacking calsequestrin revealed by a genetically encoded probe.

TL;DR: A targetable ratiometric FRET-based calcium indicator (D1ER Cameleon) allowed us to investigate SR Ca2+ dynamics and analyze the impact of calsequestrin (CSQ) on SR [Ca2+] in enzymatically dissociated flexor digitorum brevis muscle fibers from WT and CSQ-KO mice lacking isoform 1 or both isoforms.