Pancreatic Beta Cells Lack a Low Glucose and O2-inducible Mitochondrial Protein That Augments Cell Survival.
From: Department of Biochemistry and Molecular Biology, University of Chicago, and The Howard Hughes Medical Institute, 5841 South Maryland Avenue, Chicago, IL 60637, USA.
Proceedings of the National Academy of Sciences of the United States of America
- Publish Date: Jul 2006
- ISSN: 0027-8424
- Volume: 103
- Issue: 28
- Pages: 10636-41
- Medium: Print
- Language: English
- Citation (JAMA): Wang Jie, Cao Yun, Chen Ying, et al. Pancreatic Beta Cells Lack a Low Glucose and O2-inducible Mitochondrial Protein That Augments Cell Survival.. Proc. Natl. Acad. Sci. U.S.A. Jul 2006;103:10636-41
Abstract
beta cell failure is a common denominator of diabetes. Susceptibility to stress-induced apoptosis may underlie beta cell failure and/or hamper islet transplantation therapy. The causal basis is not well understood. In efforts to identify important differences in gene expression in alpha vs. beta cells, a gene termed HIMP1 (Hypoglycemia/hypoxia Inducible Mitochondrial Protein, or HIG1) has been cloned from an alpha cell cDNA library. It is a member of a well conserved eukaryote protein family. In mice, its two alternatively spliced products each form a transmembrane loop, having an N(outside)-C(outside) orientation and are expressed highly in the mitochondrial inner membrane in several tissues including heart and pancreatic alpha cells, but not in beta cells. Ectopic expression of HIMP1 in MIN6 beta cells protects the cells from apoptosis induced by several stimuli and prolongs their survival. These results suggest an important role for HIMP1 in stress protective programs in mitochondria.
Mesh Headings (Keywords): Animals, Cell Line, Tumor, Cell Survival, Glucose, Insulin-Secreting Cells, Intracellular Membranes, Membrane Proteins, Mice, Mitochondria, Mitochondrial Proteins, Molecular Sequence Data, Oxygen
Check for Full Text / PubMed Unique Identifier (PMID): 16815968
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