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The key antioxidant enzymes and transcription factor Nrf2 are up-regulated, and the NOX5 expression is reduced during development of drug resistance of tumor cells to cisplatin.
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Study shows that the bona fide nonglycoprotein Nox5, a transmembrane superoxide-producing NADPH oxidase, is transported to the cell surface in a manner resistant to co-expression of Sar1 (H79G), a GTP-fixed mutant of the small GTPase Sar1, which blocks COPII vesicle fission from the endoplasmic reticulum.
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Neoplastic cells appeared unable to downregulate NOX5 mRNA expression under leptin. Leptin emerged as a potential activator of ROS production in human epithelial mammary cells, where the ROS production was apparently linked to NOX5 activation. This novel finding could shed light on the potential role of obesity-associated hyperleptinemia in mammary cells via the activation of NOX enzymes
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The authors conclude that taurodeoxycholic acid-induced DNA damage may depend on the activation of TGR5, CREB and NOX5-S. It is possible that in Barrett's patients bile acids may activate NOX5-S and increase reactive oxygen species (ROS) production via activation of TGR5 and CREB. NOX5-S-derived ROS may cause DNA damage, thereby contributing to the progression from Barrett's esophagus to esophageal adenocarcinoma.
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western blot analysis of platelets from X-linked chronic granulomatous disease patients showed Nox5 expression with a quantity comparable to that of normal platelets
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Data suggest that NOX5 expression in melanoma cells could contribute to cell proliferation due, in part, to the generation of high local concentrations of extracellular ROS that modulate multiple pathways that regulate HIF-1alpha and networks that signal through Akt/GSK3beta/p27(Kip1) .
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We demonstrated that rapid deletion of p22phox is possible and that the activity of Nox1 and Nox4 but not Nox5 exclusively depends on p22phox.
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NOX5-p22phox complex drives monocytic differentiation into dendritic cells, and thus could be critical for immunity and inflammation.
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Data strongly suggest that oxidation of calcium-binding domain of NOX5 could be implicated in its inactivation, serving as a possible defense mechanism against oxidative stress.
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NOX5 activation played a pathophysiological role in vascular disease. [review]
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NOX5-L depletion consistently suppressed breast cancer cell proliferation, invasion, and migration in vitro. NOX5-L expression is regulated by STAT5A in breast cancer cells.
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REVIEW: recent knowledge of the genetic and enzymatic regulation of NOX5 and the importance of NOX5 in human physiology and pathophysiology.
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Rho Kinase ROCK2 Mediates Acid-Induced NADPH Oxidase NOX5-S Expression in Human Esophageal Adenocarcinoma Cells
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Nox5-derived ROS and subsequent depletion of PKCzeta and JNK inactivation play a critical role in modulating intracellular signaling cascades involved in the proliferation and survival of PCa cells.
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High glucose generated an increase in NADPH oxidase activity and expression in human vascular smooth muscle cells. Sequence analysis of human Nox1, Nox4, and Nox5 gene promoters
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These results provide new insight into the redox-dependent mechanism of HTLV-1 transformation and raises an intriguing possibility that Nox5alpha serves as a potential molecular target to treat HTLV-1-related leukemia.
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NOX5-derived reactive oxygen species contribute to apoptosis blockage in ALK-positive anaplastic large-cell lymphoma cell lines.
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Tissue microarray analysis revealed, for the first time, substantial Nox5 overexpression in several human cancers
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Initial findings suggest that glomerular and tubular expression of Nox5 is induced during diabetes and hypertension, respectively. Furthermore, identification of SNPs in distinct human populations suggests a role for either good or ill for this enzyme.
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Induction of Nox5 expression in IFNgamma- and oxidized LDL-exposed Mac and the presence of Nox5 in Mac-rich atheroma are indicative of the implication of Nox5 in atherogenesis.
