Professor, Medicine, University of Alabama School of Medicine
Endocrinology
Dr. Anath Shalev, MD
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Anath Shalev practices Endocrinology. Dr. Anath Shalev is a published doctor. He published 31 publications, including: '-Cell MicroRNAs: Small but Powerful.'
Publications
- β-Cell MicroRNAs: Small but Powerful.
- MicroRNA-200 Is Induced by Thioredoxin-interacting Protein and Regulates Zeb1 Protein Signaling and Beta Cell Apoptosis.
- Thioredoxin-Interacting Protein: Regulation and Function in the Pancreatic Beta Cell.
- Thioredoxin-Interacting Protein Stimulates its Own Expression via a Positive Feedback Loop.
- Thioredoxin-interacting protein regulates insulin transcription through microRNA-204.
- FOXO1 Competes with Carbohydrate Response Element-binding Protein (ChREBP) and Inhibits Thioredoxin-interacting Protein (TXNIP) Transcription in Pancreatic Beta Cells.
- A proinsulin gene splice variant with increased translation efficiency is expressed in human pancreatic islets.
- Oligonucleotide microarray analysis of intact human pancreatic islets: identification of glucose-responsive genes and a highly regulated TGFbeta signaling pathway.
- Resistin is expressed in pancreatic islets.
- Peak stimulated insulin secretion is associated with specific changes in gene expression profiles in sporadic insulinomas.
- Resistin serum levels in type 1 diabetes pre- and post-islet transplantation.
- Insulinomas and expression of an insulin splice variant.
- Increased insulin translation from an insulin splice-variant overexpressed in diabetes, obesity, and insulin resistance.
- Thioredoxin-interacting protein is stimulated by glucose through a carbohydrate response element and induces beta-cell apoptosis.
- Gene expression profiling in INS-1 cells overexpressing thioredoxin-interacting protein.
- Exenatide inhibits beta-cell apoptosis by decreasing thioredoxin-interacting protein.
- Metabolism-independent sugar effects on gene transcription: the role of 3-O-methylglucose.
- Nitric oxide-dependent suppression of thioredoxin-interacting protein expression enhances thioredoxin activity.
- An analysis of high glucose and glucosamine-induced gene expression and oxidative stress in renal mesangial cells.
- A cis-element in the 5' untranslated region of the preproinsulin mRNA (ppIGE) is required for glucose regulation of proinsulin translation.
- Exenatide blocks JAK1-STAT1 in pancreatic beta cells.
- Thioredoxin-interacting protein: a critical link between glucose toxicity and beta-cell apoptosis.
- HIV-protease inhibitors induce expression of suppressor of cytokine signaling-1 in insulin-sensitive tissues and promote insulin resistance and type 2 diabetes mellitus.
- Thioredoxin-interacting protein deficiency induces Akt/Bcl-xL signaling and pancreatic beta-cell mass and protects against diabetes.
- Lack of TXNIP protects beta-cells against glucotoxicity.
- Diabetes induces and calcium channel blockers prevent cardiac expression of proapoptotic thioredoxin-interacting protein.
- Glucose-stimulated expression of Txnip is mediated by carbohydrate response element-binding protein, p300, and histone H4 acetylation in pancreatic beta cells.
- Lack of TXNIP protects against mitochondria-mediated apoptosis but not against fatty acid-induced ER stress-mediated beta-cell death.
- Intracellular shuttling and mitochondrial function of thioredoxin-interacting protein.
- Enhanced MIN-6 beta cell survival and function on a nitric oxide-releasing peptide amphiphile nanomatrix.
Doctors Specialties
- Endocrinology
Accepted Insurances
Education
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National Institutes of Health Clinical Center -
University of Basel Faculty of Medicine
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