Maria S. Remedi

HIV protease inhibitors acutely impair glucose-stimulated insulin release.

Remodeling of excitation-contraction coupling in transgenic mice expressing ATP-insensitive sarcolemmal KATP channels.

Signaling elements involved in the metabolic regulation of mTOR by nutrients, incretins, and growth factors in islets.

Diet-induced glucose intolerance in mice with decreased beta-cell ATP-sensitive K+ channels.

Transgenic overexpression of SUR1 in the heart suppresses sarcolemmal K(ATP).

ATP and sulfonylurea sensitivity of mutant ATP-sensitive K+ channels in neonatal diabetes: implications for pharmacogenomic therapy.

ATP-sensitive K+ channel signaling in glucokinase-deficient diabetes.

Glucose-stimulated DNA synthesis through mammalian target of rapamycin (mTOR) is regulated by KATP channels: effects on cell cycle progression in rodent islets.

Critical role of gap junction coupled KATP channel activity for regulated insulin secretion.

Hyperinsulinism in mice with heterozygous loss of K(ATP) channels.

Expression of ATP-insensitive KATP channels in pancreatic beta-cells underlies a spectrum of diabetic phenotypes.

Chronic antidiabetic sulfonylureas in vivo: reversible effects on mouse pancreatic beta-cells.

Ca2+-independent alterations in diastolic sarcomere length and relaxation kinetics in a mouse model of lipotoxic diabetic cardiomyopathy.

Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus.

K(ATP) channelopathies in the pancreas.

Hyperinsulinism and diabetes: genetic dissection of beta cell metabolism-excitation coupling in mice.

HMR 1098 is not an SUR isotype specific inhibitor of heterologous or sarcolemmal K ATP channels.

Acute sulfonylurea therapy at disease onset can cause permanent remission of KATP-induced diabetes.

Hypotension due to Kir6.1 gain-of-function in vascular smooth muscle.

Pancreatic β cell dedifferentiation in diabetes and redifferentiation following insulin therapy.

Mitochondrial pyruvate carrier 2 hypomorphism in mice leads to defects in glucose-stimulated insulin secretion.

Remission of severe neonatal diabetes with very early sulfonylurea treatment.

Pancreatic β-cell identity in diabetes.

An ancestral role for the mitochondrial pyruvate carrier in glucose-stimulated insulin secretion.

Rpl13a small nucleolar RNAs regulate systemic glucose metabolism.

Diabetes induced by gain-of-function mutations in the Kir6.1 subunit of the KATP channel.

Should I Stay or Should I Go: A Clash of α-Cell Identity.

Intermittent fasting preserves beta-cell mass in obesity-induced diabetes via the autophagy-lysosome pathway.

High-fat-diet-induced remission of diabetes in a subset of K -GOF insulin-secretory-deficient mice.

Cardiovascular consequences of KATP overactivity in Cantu syndrome.

In vivo monitoring of intracellular Ca dynamics in the pancreatic β-cells of zebrafish embryos.

The role of membrane excitability in pancreatic β-cell glucotoxicity.

ABCC9-related Intellectual disability Myopathy Syndrome is a K channelopathy with loss-of-function mutations in ABCC9.

Glibenclamide reverses cardiovascular abnormalities of Cantu syndrome driven by KATP channel overactivity.

Cantú syndrome: Findings from 74 patients in the International Cantú Syndrome Registry.

Kir6.1-dependent K channels in lymphatic smooth muscle and vessel dysfunction in mice with Kir6.1 gain-of-function.

Alterations in pancreatic islet cell function in response to small bowel resection.

The Mechanism of High-Output Cardiac Hypertrophy Arising From Potassium Channel Gain-of-Function in Cantú Syndrome.

Kir6.1- and SUR2-dependent KATP overactivity disrupts intestinal motility in murine models of Cantú syndrome.

Preferential Gq signaling in diabetes: an electrical switch in incretin action and in diabetes progression?

Complex consequences of Cantu syndrome SUR2 variant R1154Q in genetically modified mice.

Gain-of-Function Lrp5 Mutation Improves Bone Mass and Strength and Delays Hyperglycemia in a Mouse Model of Insulin-Deficient Diabetes.

Cognitive deficits and impaired hippocampal long-term potentiation in K-induced DEND syndrome.

ATP-Sensitive Potassium Channels in Hyperinsulinism and Type 2 Diabetes: Inconvenient Paradox or New Paradigm?

Genetic Reduction of Glucose Metabolism Preserves Functional β-Cell Mass in KATP-Induced Neonatal Diabetes.

A Unique High-Output Cardiac Hypertrophy Phenotype Arising From Low Systemic Vascular Resistance in Cantu Syndrome.

Glucokinase Inhibition: A Novel Treatment for Diabetes?

KATP channels are necessary for glucose-dependent increases in amyloid-β and Alzheimer's disease-related pathology.

Intermittent fasting protects β-cell identity and function in a type-2 diabetes model.