Regulation of NOX-1 expression in beta cells: A positive feedback loop involving the Src-kinase signaling pathway

► Pro-inflammatory cytokines induce NADPH oxidase-1 expression in beta cells. ► Inhibitors of NADPH oxidase block NOX-1 expression in beta cells. ► Cellular reactive oxygen species levels modulate NOX-1 expression in beta cells. ► Src-kinase activation by cellular reactive oxygen species activates N...

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Bibliographic Details
Published in:Molecular and cellular endocrinology 2013-04, Vol.369 (1-2), p.35-41
Main Authors: Weaver, J.R., Taylor-Fishwick, D.A.
Format: Article
Language:English
Subjects:
antioxidants
Apoptosis
Beta cells
cell death
Cell Line
Cell Survival
Cytokines
Diabetes
Feed-forward regulation
Feedback, Physiological
Gene Expression Regulation
Humans
inflammation
insulin secretion
Insulin-Secreting Cells - cytology
Insulin-Secreting Cells - enzymology
NAD(P)H oxidase (H2O2-forming)
NADH, NADPH Oxidoreductases - metabolism
NADPH Oxidase 1
reactive oxygen species
Reactive Oxygen Species - metabolism
Signal Transduction
src-Family Kinases - antagonists & inhibitors
src-Family Kinases - metabolism
Src-kinase
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Summary:► Pro-inflammatory cytokines induce NADPH oxidase-1 expression in beta cells. ► Inhibitors of NADPH oxidase block NOX-1 expression in beta cells. ► Cellular reactive oxygen species levels modulate NOX-1 expression in beta cells. ► Src-kinase activation by cellular reactive oxygen species activates NOX-1 expression. ► Feedback regulation of NOX-1 in β-cells, an enticing therapeutic target in diabetes. NADPH oxidase-1 (NOX-1) is upregulated in beta cells in response to pro-inflammatory cytokines. Inhibition of NADPH oxidase activity blocked stimulated NOX-1 expression (p
ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2013.01.011