Salvatore Mancarella

Promotion of regeneration of corticospinal tract axons in rats with recombinant vascular endothelial growth factor alone and combined with adenovirus coding for this factor.

Sugar-induced modification of fibroblast growth factor 2 reduces its angiogenic activity in vivo.

Paradoxical effect of dofetilide on action potential duration and calcium transient amplitude in newborn rabbit ventricular myocytes.

Stabilization of cardiac ryanodine receptor prevents intracellular calcium leak and arrhythmias.

Impaired Ca2+ homeostasis is associated with atrial fibrillation in the alpha1D L-type Ca2+ channel KO mouse.

STIM protein coupling in the activation of Orai channels.

Silencing of Cav1.2 gene in neonatal cardiomyocytes by lentiviral delivered shRNA.

The short N-terminal domains of STIM1 and STIM2 control the activation kinetics of Orai1 channels.

Congenital heart block: identification of autoantibody binding site on the extracellular loop (domain I, S5-S6) of alpha(1D) L-type Ca channel.

Calcium signals: STIM dynamics mediate spatially unique oscillations.

The calcium store sensor, STIM1, reciprocally controls Orai and CaV1.2 channels.

Rescue and worsening of congenital heart block-associated electrocardiographic abnormalities in two transgenic mice.

Signal transduction: STIM1 senses both Ca²+ and heat.

Hypoxia-induced acidosis uncouples the STIM-Orai calcium signaling complex.

Gene disruption of the calcium channel Orai1 results in inhibition of osteoclast and osteoblast differentiation and impairs skeletal development.

Targeted STIM deletion impairs calcium homeostasis, NFAT activation, and growth of smooth muscle.

Blockade of NOX2 and STIM1 signaling limits lipopolysaccharide-induced vascular inflammation.

Distinct Orai-coupling domains in STIM1 and STIM2 define the Orai-activating site.

Myofibroblast secretome and its auto-/paracrine signaling.

Atrophied cardiomyocytes and their potential for rescue and recovery of ventricular function.

STIM1-dependent Ca(2+) microdomains are required for myofilament remodeling and signaling in the heart.