Marco Brotto

Influence of ageing on the fatigability of isolated mouse skeletal muscles from mature and aged mice.

Truncation by Glu180 nonsense mutation results in complete loss of slow skeletal muscle troponin T in a lethal nemaline myopathy.

Troponin T isoforms alter the tolerance of transgenic mouse cardiac muscle to acidosis.

Defective maintenance of intracellular Ca2+ homeostasis is linked to increased muscle fatigability in the MG29 null mice.

Functional and biochemical modifications in skeletal muscles from malarial mice.

Uncontrolled calcium sparks act as a dystrophic signal for mammalian skeletal muscle.

Enhanced resistance to fatigue and altered calcium handling properties of sarcalumenin knockout mice.

Coupled expression of troponin T and troponin I isoforms in single skeletal muscle fibers correlates with contractility.

Uncoupling store-operated Ca2+ entry and altered Ca2+ release from sarcoplasmic reticulum through silencing of junctophilin genes.

Muscle aging is associated with compromised Ca2+ spark signaling and segregated intracellular Ca2+ release.

Azumolene inhibits a component of store-operated calcium entry coupled to the skeletal muscle ryanodine receptor.

Compromised store-operated Ca2+ entry in aged skeletal muscle.

MG53 nucleates assembly of cell membrane repair machinery.

Deficiency of MIP/MTMR14 phosphatase induces a muscle disorder by disrupting Ca(2+) homeostasis.

Temporal adaptive changes in contractility and fatigability of diaphragm muscles from streptozotocin-diabetic rats.

Muscle-specific inositide phosphatase (MIP/MTMR14) is reduced with age and its loss accelerates skeletal muscle aging process by altering calcium homeostasis.

Ca2+ overload and sarcoplasmic reticulum instability in tric-a null skeletal muscle.

Phosphatidylinositol 3,5-bisphosphate (PI(3,5)P2) potentiates cardiac contractility via activation of the ryanodine receptor.

Phosphatidylinositol 3,5-bisphosphate increases intracellular free Ca2+ in arterial smooth muscle cells and elicits vasocontraction.

Store-operated Ca(2+) entry (SOCE) contributes to normal skeletal muscle contractility in young but not in aged skeletal muscle.

Disrupted membrane structure and intracellular Ca²⁺ signaling in adult skeletal muscle with acute knockdown of Bin1.

Store-operated calcium entry is present in HL-1 cardiomyocytes and contributes to resting calcium.

Aging, sarcopenia and store-operated calcium entry: A common link?

Kruppel-like factor 15 regulates skeletal muscle lipid flux and exercise adaptation.

Sarcopenia: Pharmacology today and tomorrow.

Application of the m technique in hospitalized very preterm infants: a feasibility study.

Prostaglandin E2: From Clinical Applications to Its Potential Role in Bone-Muscle Crosstalk and Myogenic Differentiation.

Jatropha curcas: From Biodiesel Generation to Medicinal Applications.

Hyperthermia: From Diagnostic and Treatments to New Discoveries.