NCB5OR DEFICIENCY INCREASES FATTY ACID CATABOLISM, OXIDATIVE STRESS
Washington University, Saint Louis MO
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Abstract
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. NADH cytochrome b5 oxidoreductase (Ncb5or) is an endoplasmic reticulum-associated redox protein that is widely distributed in animal tissues. Ncb5or-/- mice develop diabetes at age 7 weeks and have increased susceptibility to the diabetogenic effects of the b-cell toxin streptozotocin. Ncb5or deficiency also results in lipoatrophy and increased hepatocyte sensitivity to cytotoxic effects of saturated fatty acids.
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