Florent Allagnat

[Gap functions and diseases].

[Gap junctions and secretion].

Glucose represses connexin36 in insulin-secreting cells.

ICER-1gamma overexpression drives palmitate-mediated connexin36 down-regulation in insulin-secreting cells.

Connexins, diabetes and the metabolic syndrome.

Plasma membrane Ca2+-ATPase overexpression depletes both mitochondrial and endoplasmic reticulum Ca2+ stores and triggers apoptosis in insulin-secreting BRIN-BD11 cells.

Heterozygous inactivation of the Na/Ca exchanger increases glucose-induced insulin release, β-cell proliferation, and mass.

Exposure to the viral by-product dsRNA or Coxsackievirus B5 triggers pancreatic beta cell apoptosis via a Bim / Mcl-1 imbalance.

Connexins protect mouse pancreatic β cells against apoptosis.

HDLs protect pancreatic β-cells against ER stress by restoring protein folding and trafficking.

Cx36 is a target of Beta2/NeuroD1, which associates with prenatal differentiation of insulin-producing β cells.

Specific silencing of the REST target genes in insulin-secreting cells uncovers their participation in beta cell survival.

Reduction of connexin36 content by ICER-1 contributes to insulin-secreting cells apoptosis induced by oxidized LDL particles.

Connexins and M3 muscarinic receptors contribute to heterogeneous Ca(2+) signaling in mouse aortic endothelium.

Hyperglycemia downregulates Connexin36 in pancreatic islets via the upregulation of ICER-1/ICER-1γ.

The use of external mesh reinforcement to reduce intimal hyperplasia and preserve the structure of human saphenous veins.