Homologs of gp91 phox : cloning and tissue expression of Nox3, Nox4, and Nox5

Cheng, Guangjie; Cao, Zehong; Xu, Xiaojin; Meir, Erwin G. Van; Lambeth, J. David

doi:10.1016/s0378-1119(01)00449-8

Cited by 738 publications

(661 citation statements)

References 19 publications

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“…Furthermore, expression of Nox4 was also detected in renal cell carcinoma (Shiose et al, 2001) and glioblastoma (Cheng et al, 2001), implying the possible role of Nox4-generated ROS in maintenance of transformation phenotypes. We have recently found that Nox1 is functionally required for maintenance of Ras-induced transformation phenotypes (Mitsushita et al, 2004).…”

Section: Discussionmentioning

confidence: 95%

Inhibition of NADPH oxidase 4 activates apoptosis via the AKT/apoptosis signal-regulating kinase 1 pathway in pancreatic cancer PANC-1 cells

et al. 2006

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Pancreatic adenocarcinoma is an aggressive human malignancy and is characterized by resistance to apoptosis. Recently, NADPH oxidase (Nox) 4-mediated generation of intracellular reactive oxygen species (ROS) was proposed to confer antiapoptotic activity and thus a growth advantage to pancreatic cancer cells. The signaling mechanism by which Nox4 transmits cell survival signals remains unclear. Here, we show that both a flavoprotein inhibitor, diphenylene iodonium (DPI), and small interfering RNAs designed to target Nox4 mRNA (siNox4R-NAs) inhibited superoxide production in PANC-1 pancreatic cancer cells, and depletion of ROS by DPI or siNox4RNAs induced apoptosis. Parallely, DPI treatment and siNox4RNA transfection blocked activation of the cell survival kinase AKT by attenuating phosphorylation of AKT. Furthermore, AKT phosphorylation of apoptosis signal-regulating kinase 1 (ASK1) on Ser-83 was reduced by DPI and siNox4RNAs. When ASK1Ser83Ala (an AKT phosphorylation-defective ASK1 mutant) was introduced into PANC-1 cells, this mutant alone induced apoptosis. But, addition of DPI or co-transfection of siNox4RNA had no additive effect, indicating that the mutant can substitute for these reagents in apoptosis induction. Taken together, these findings suggest that ROS generated by Nox4, at least in part, transmit cell survival signals through the AKT-ASK1 pathway in pancreatic cancer cells and their depletion leads to apoptosis.

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Section: Discussionmentioning

confidence: 95%

Inhibition of NADPH oxidase 4 activates apoptosis via the AKT/apoptosis signal-regulating kinase 1 pathway in pancreatic cancer PANC-1 cells

et al. 2006

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“…In many of cases, the source of this ROS is Nox enzymes: this includes melanoma (Nox4, [127]), prostate cancer (Nox5 [128] and Nox1 [129]), glioblastoma (Nox4 and sometimes Nox5 [130]), H. pylorusinduced gastric inflammation leading to gastric cancer (Nox1 [131]) and Barrett's esophageal adenocarcinoma (Nox5 [132]). Some, but not all reports have observed an increase in Nox1 expression in colon cancer, see [133][134][135][136].…”

Section: A Association Of Ros Nox Enzymes and Cancermentioning

confidence: 99%

Nox enzymes, ROS, and chronic disease: An example of antagonistic pleiotropy

Lambeth¹

2007

Free Radical Biology and Medicine

578

446

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“…Analysis of total lung or airway mRNA revealed the presence of substantial amounts of NOX2 as well as DUOX1 and DUOX2, and low amounts of NOX1 and NOX4 (35,(79)(80)(81). Although expression of NOX originates primarily from alveolar macrophages and other inflammatory cell types, the other NOX/DUOX enzymes are largely expressed in non-phagocytic cells within the lung, including airway and alveolar epithelial cells, pulmonary endothelial cells, fibroblasts, and smooth muscle cells.…”

Section: Nox Isozymes Within the Respiratory Tractmentioning

confidence: 99%

NADPH oxidases in lung biology and pathology: Host defense enzymes, and more

Vliet

2008

Free Radical Biology and Medicine

186

191

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The deliberate production of reactive oxygen species (ROS) by phagocyte NADPH oxidase is widely appreciated as a critical component of antimicrobial host defense. Recently, additional homologs of NADPH oxidase (NOX) have been discovered throughout the animal and plant kingdoms, which appear to possess diverse functions in addition to host defense, including cell proliferation, differentiation, and regulation of gene expression. Several of these NOX homologs are also expressed within the respiratory tract, where they participate in innate host defense as well as in epithelial and inflammatory cell signaling and gene expression, and fibroblast and smooth muscle cell proliferation, in response to bacterial or viral infection and environmental stress. Inappropriate expression or activation of NOX/DUOX during various lung pathologies suggests their specific involvement in respiratory disease. This review summarizes the current state of knowledge regarding the general functional properties of mammalian NOX enzymes, and their specific importance in respiratory tract physiology and pathology.

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Homologs of gp91 phox : cloning and tissue expression of Nox3, Nox4, and Nox5

Cited by 738 publications

References 19 publications

Inhibition of NADPH oxidase 4 activates apoptosis via the AKT/apoptosis signal-regulating kinase 1 pathway in pancreatic cancer PANC-1 cells

Inhibition of NADPH oxidase 4 activates apoptosis via the AKT/apoptosis signal-regulating kinase 1 pathway in pancreatic cancer PANC-1 cells

Nox enzymes, ROS, and chronic disease: An example of antagonistic pleiotropy

NADPH oxidases in lung biology and pathology: Host defense enzymes, and more

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