PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33279617-8 2021 siRNA-mediated down-regulation of NOX1 or NOX4 inhibited NOD1-mediated ROS production and increased the expression of antioxidant defense enzyme catalase and superoxide dismutase (SOD). Reactive Oxygen Species 71-74 NADPH oxidase 1 Homo sapiens 34-38 33548451-2 2021 Platelet NADPH oxidase-1 (Nox-1) contributes to ROS generation and thrombus formation downstream of the collagen receptor GPVI. Reactive Oxygen Species 48-51 NADPH oxidase 1 Homo sapiens 9-24 33548451-2 2021 Platelet NADPH oxidase-1 (Nox-1) contributes to ROS generation and thrombus formation downstream of the collagen receptor GPVI. Reactive Oxygen Species 48-51 NADPH oxidase 1 Homo sapiens 26-31 33446567-0 2021 An interplay of NOX1-derived ROS and oxygen determines the spermatogonial stem cell self-renewal efficiency under hypoxia. Reactive Oxygen Species 29-32 NADPH oxidase 1 Homo sapiens 16-20 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 42-58 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 60-64 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 187-191 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 25-28 NADPH oxidase 1 Homo sapiens 42-58 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 25-28 NADPH oxidase 1 Homo sapiens 60-64 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 25-28 NADPH oxidase 1 Homo sapiens 187-191 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 166-169 NADPH oxidase 1 Homo sapiens 42-58 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 166-169 NADPH oxidase 1 Homo sapiens 60-64 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 166-169 NADPH oxidase 1 Homo sapiens 187-191 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 166-169 NADPH oxidase 1 Homo sapiens 42-58 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 166-169 NADPH oxidase 1 Homo sapiens 60-64 33446567-1 2021 Reactive oxygen species (ROS) produced by NADPH1 oxidase 1 (NOX1) are thought to drive spermatogonial stem cell (SSC) self-renewal through feed-forward production of ROS by the ROS-BCL6B-NOX1 pathway. Reactive Oxygen Species 166-169 NADPH oxidase 1 Homo sapiens 187-191 33446567-9 2021 On the other hand, chemical suppression of mitochondria-derived ROS or Top1mt mitochondria-specific topoisomerase deficiency did not influence SSC fate, suggesting that NOX1-derived ROS play a more important role in SSCs than mitochondria-derived ROS. Reactive Oxygen Species 182-185 NADPH oxidase 1 Homo sapiens 169-173 33446567-9 2021 On the other hand, chemical suppression of mitochondria-derived ROS or Top1mt mitochondria-specific topoisomerase deficiency did not influence SSC fate, suggesting that NOX1-derived ROS play a more important role in SSCs than mitochondria-derived ROS. Reactive Oxygen Species 182-185 NADPH oxidase 1 Homo sapiens 169-173 32780286-13 2021 Moreover, novel non-ROS-related proteins were part of these forming functional hybrids, such as the NOX5/sGC, NOX1,2/NOS2, NRF2/ENC-1 and MPO/SP-A modules. Reactive Oxygen Species 20-23 NADPH oxidase 1 Homo sapiens 110-114 33968728-0 2021 DDX19A Promotes Metastasis of Cervical Squamous Cell Carcinoma by Inducing NOX1-Mediated ROS Production. Reactive Oxygen Species 89-92 NADPH oxidase 1 Homo sapiens 75-79 33968728-8 2021 Our results demonstrated that DDX19A could promote CSCC metastasis by inducing NOX1-mediated ROS production and that blockage of the NOX1/ROS axis might serve as a potential therapeutic target for patients with DDX19A-overexpressed CSCC. Reactive Oxygen Species 93-96 NADPH oxidase 1 Homo sapiens 79-83 33968728-8 2021 Our results demonstrated that DDX19A could promote CSCC metastasis by inducing NOX1-mediated ROS production and that blockage of the NOX1/ROS axis might serve as a potential therapeutic target for patients with DDX19A-overexpressed CSCC. Reactive Oxygen Species 138-141 NADPH oxidase 1 Homo sapiens 133-137 32767144-8 2021 The only professional primary ROS producers are NADPH oxidases (NOX1-5, DUOX1-2). Reactive Oxygen Species 30-33 NADPH oxidase 1 Homo sapiens 64-68 30334629-1 2019 SIGNIFICANCE: NADPH oxidases (Noxs), of which there are seven isoforms (Nox1-5, Duox1/Duox2), are professional oxidases functioning as reactive oxygen species (ROS)-generating enzymes. Reactive Oxygen Species 135-158 NADPH oxidase 1 Homo sapiens 72-76 32961197-1 2020 NADPH oxidases 1 (NOX1) derived reactive oxygen species (ROS) play an important role in the progression of cancer through signaling pathways. Reactive Oxygen Species 32-55 NADPH oxidase 1 Homo sapiens 0-16 32961197-1 2020 NADPH oxidases 1 (NOX1) derived reactive oxygen species (ROS) play an important role in the progression of cancer through signaling pathways. Reactive Oxygen Species 32-55 NADPH oxidase 1 Homo sapiens 18-22 32961197-1 2020 NADPH oxidases 1 (NOX1) derived reactive oxygen species (ROS) play an important role in the progression of cancer through signaling pathways. Reactive Oxygen Species 57-60 NADPH oxidase 1 Homo sapiens 0-16 32961197-1 2020 NADPH oxidases 1 (NOX1) derived reactive oxygen species (ROS) play an important role in the progression of cancer through signaling pathways. Reactive Oxygen Species 57-60 NADPH oxidase 1 Homo sapiens 18-22 31173656-7 2020 Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death. Reactive Oxygen Species 216-219 NADPH oxidase 1 Homo sapiens 138-142 31173656-7 2020 Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death. Reactive Oxygen Species 227-230 NADPH oxidase 1 Homo sapiens 138-142 30801870-9 2019 ABSTRACT: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), comprise seven family members (Nox1-Nox5 and dual oxidase 1 and 2) and are major producers of reactive oxygen species in mammalian cells. Reactive Oxygen Species 172-195 NADPH oxidase 1 Homo sapiens 109-113 30690057-0 2019 ROS-generating oxidase NOX1 promotes the self-renewal activity of CD133+ thyroid cancer cells through activation of the Akt signaling. Reactive Oxygen Species 0-3 NADPH oxidase 1 Homo sapiens 23-27 30690057-5 2019 The transcriptional level of ROS-generating oxidase NADPH oxidase 1 (NOX1) is high in CD133 + thyroid cancer cells. Reactive Oxygen Species 29-32 NADPH oxidase 1 Homo sapiens 52-67 30690057-5 2019 The transcriptional level of ROS-generating oxidase NADPH oxidase 1 (NOX1) is high in CD133 + thyroid cancer cells. Reactive Oxygen Species 29-32 NADPH oxidase 1 Homo sapiens 69-73 30690057-7 2019 Knock down of NOX1 obviously reduced the level of ROS and inhibited the self-renewal activity and tumorigenicity of CD133 + thyroid cancer cells. Reactive Oxygen Species 50-53 NADPH oxidase 1 Homo sapiens 14-18 32856850-2 2020 Enzymes such as xanthine oxidase (XO) and NADPH oxidase 1 (NOX1) as relevant sources of reactive oxygen species (ROS) production may play a crucial role in the incidence and progress of MM. Reactive Oxygen Species 88-111 NADPH oxidase 1 Homo sapiens 42-57 32856850-2 2020 Enzymes such as xanthine oxidase (XO) and NADPH oxidase 1 (NOX1) as relevant sources of reactive oxygen species (ROS) production may play a crucial role in the incidence and progress of MM. Reactive Oxygen Species 88-111 NADPH oxidase 1 Homo sapiens 59-63 32856850-2 2020 Enzymes such as xanthine oxidase (XO) and NADPH oxidase 1 (NOX1) as relevant sources of reactive oxygen species (ROS) production may play a crucial role in the incidence and progress of MM. Reactive Oxygen Species 113-116 NADPH oxidase 1 Homo sapiens 42-57 32856850-2 2020 Enzymes such as xanthine oxidase (XO) and NADPH oxidase 1 (NOX1) as relevant sources of reactive oxygen species (ROS) production may play a crucial role in the incidence and progress of MM. Reactive Oxygen Species 113-116 NADPH oxidase 1 Homo sapiens 59-63 32640089-6 2020 By inhibiting NOX1, stress related signalling cascades and elevated ROS levels could be abrogated, and survival of AD and PSO cells improved. Reactive Oxygen Species 68-71 NADPH oxidase 1 Homo sapiens 14-18 32064493-2 2020 NOX1 has been recently recognized as a major source of reactive oxygen species (ROS) in human colonic epithelial cells. Reactive Oxygen Species 55-78 NADPH oxidase 1 Homo sapiens 0-4 32064493-2 2020 NOX1 has been recently recognized as a major source of reactive oxygen species (ROS) in human colonic epithelial cells. Reactive Oxygen Species 80-83 NADPH oxidase 1 Homo sapiens 0-4 32064493-6 2020 Our studies confirmed that loss-of-function of NOX1 causes abrogated ROS activity, but they also provided novel mechanistic insights into human NOX1 deficiency. Reactive Oxygen Species 69-72 NADPH oxidase 1 Homo sapiens 47-51 31129114-0 2019 ML171, a specific inhibitor of NOX1 attenuates formalin induced nociceptive sensitization by inhibition of ROS mediated ERK1/2 signaling. Reactive Oxygen Species 107-110 NADPH oxidase 1 Homo sapiens 31-35 30925081-14 2019 In response to TNFalpha, ASK1 is activated by Nox1-derived oxidants, and this plays a critical role in translating these ROS into a physiologic response in VSMCs. Reactive Oxygen Species 121-124 NADPH oxidase 1 Homo sapiens 46-50 30334629-1 2019 SIGNIFICANCE: NADPH oxidases (Noxs), of which there are seven isoforms (Nox1-5, Duox1/Duox2), are professional oxidases functioning as reactive oxygen species (ROS)-generating enzymes. Reactive Oxygen Species 160-163 NADPH oxidase 1 Homo sapiens 72-76 30732873-6 2019 Cerium(III) could enhance the expression and activity of NADPH oxidase1 (Nox1) leading to the elevation of intracellular reactive oxygen species (ROS) level. Reactive Oxygen Species 121-144 NADPH oxidase 1 Homo sapiens 57-71 30732873-6 2019 Cerium(III) could enhance the expression and activity of NADPH oxidase1 (Nox1) leading to the elevation of intracellular reactive oxygen species (ROS) level. Reactive Oxygen Species 121-144 NADPH oxidase 1 Homo sapiens 73-77 30732873-6 2019 Cerium(III) could enhance the expression and activity of NADPH oxidase1 (Nox1) leading to the elevation of intracellular reactive oxygen species (ROS) level. Reactive Oxygen Species 146-149 NADPH oxidase 1 Homo sapiens 57-71 30732873-6 2019 Cerium(III) could enhance the expression and activity of NADPH oxidase1 (Nox1) leading to the elevation of intracellular reactive oxygen species (ROS) level. Reactive Oxygen Species 146-149 NADPH oxidase 1 Homo sapiens 73-77 29441570-5 2018 At pharmacologically relevant concentrations, the Nox1/Nox4 inhibitor GKT137831 attenuated ROS production, CAF-associated marker expression and migration of TGFbeta1-activated but not nonactivated primary human prostate fibroblasts. Reactive Oxygen Species 91-94 NADPH oxidase 1 Homo sapiens 50-54 30755243-0 2019 SHMT1 inhibits the metastasis of HCC by repressing NOX1-mediated ROS production. Reactive Oxygen Species 65-68 NADPH oxidase 1 Homo sapiens 51-55 30755243-16 2019 CONCLUSIONS: These data indicate that SHMT1 inhibits the metastasis of HCC by repressing NOX1 mediated ROS production. Reactive Oxygen Species 103-106 NADPH oxidase 1 Homo sapiens 89-93 29478325-0 2019 Carcinogenesis and Reactive Oxygen Species Signaling: Interaction of the NADPH Oxidase NOX1-5 and Superoxide Dismutase 1-3 Signal Transduction Pathways. Reactive Oxygen Species 19-42 NADPH oxidase 1 Homo sapiens 87-93 30146064-10 2018 In conclusion, TA can protecte the megakaryocytes from apoptosis caused by IR through inhibiting Nox1 expression to reduce ROS generation and repressing JNK/p38 MAPK pathway activation. Reactive Oxygen Species 123-126 NADPH oxidase 1 Homo sapiens 97-101 30279516-0 2019 NOX1-derived ROS drive the expression of Lipocalin-2 in colonic epithelial cells in inflammatory conditions. Reactive Oxygen Species 13-16 NADPH oxidase 1 Homo sapiens 0-4 30279516-2 2019 The major source of ROS in intestinal epithelial cells is the NADPH oxidase NOX1, which consists of the transmembrane proteins, NOX1 and p22PHOX, and the cytosolic proteins, NOXO1, NOXA1, and Rac1. Reactive Oxygen Species 20-23 NADPH oxidase 1 Homo sapiens 76-80 30279516-2 2019 The major source of ROS in intestinal epithelial cells is the NADPH oxidase NOX1, which consists of the transmembrane proteins, NOX1 and p22PHOX, and the cytosolic proteins, NOXO1, NOXA1, and Rac1. Reactive Oxygen Species 20-23 NADPH oxidase 1 Homo sapiens 128-132 30279516-5 2019 NOX1-derived ROS drive the expression of LCN-2 by controlling the expression of IkappaBzeta, a master inducer of LCN-2. Reactive Oxygen Species 13-16 NADPH oxidase 1 Homo sapiens 0-4 29467671-1 2018 The participation of reactive oxygen species (ROS) generated by NOX1 and NOX2/NADPH oxidase has been documented during inflammatory pain. Reactive Oxygen Species 21-44 NADPH oxidase 1 Homo sapiens 64-68 29269607-1 2018 Reactive oxygen species (ROS) generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox)1 mediate cellular signalings involved in normal physiological processes, and aberrant control of Nox1 has been implicated in the pathogenesis of various diseases. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 112-117 29269607-1 2018 Reactive oxygen species (ROS) generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox)1 mediate cellular signalings involved in normal physiological processes, and aberrant control of Nox1 has been implicated in the pathogenesis of various diseases. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 214-218 29269607-1 2018 Reactive oxygen species (ROS) generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox)1 mediate cellular signalings involved in normal physiological processes, and aberrant control of Nox1 has been implicated in the pathogenesis of various diseases. Reactive Oxygen Species 25-28 NADPH oxidase 1 Homo sapiens 112-117 29269607-1 2018 Reactive oxygen species (ROS) generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox)1 mediate cellular signalings involved in normal physiological processes, and aberrant control of Nox1 has been implicated in the pathogenesis of various diseases. Reactive Oxygen Species 25-28 NADPH oxidase 1 Homo sapiens 214-218 29269607-5 2018 Furthermore, NOS31 was found to selectively inhibit Nox1-mediated ROS generation, with only a marginal effect on other Nox isoforms (Nox2-5) and no ROS scavenging activity. Reactive Oxygen Species 66-69 NADPH oxidase 1 Homo sapiens 52-56 29091079-6 2018 Within colonic crypts, NOX1 constitutively generates a high level of ROS in the crypt lumen. Reactive Oxygen Species 69-72 NADPH oxidase 1 Homo sapiens 23-27 29091079-9 2018 Our results implicate that variants in NOX1 change brush border ROS within colonic crypts at the interface between the epithelium and luminal microbes. Reactive Oxygen Species 64-67 NADPH oxidase 1 Homo sapiens 39-43 29872728-4 2018 Here, we show that Nox1 is involved in UVB-induced p38/MAPK activation and cytotoxicity via ROS generation in keratinocytes. Reactive Oxygen Species 92-95 NADPH oxidase 1 Homo sapiens 19-23 29872728-5 2018 Nox1 knockdown or inhibitor decreased UVB-induced ROS production in human keratinocytes. Reactive Oxygen Species 50-53 NADPH oxidase 1 Homo sapiens 0-4 29872728-12 2018 Collectively, these data suggest that Nox1-mediated ROS production is required for UVB-induced cytotoxicity and inflammation through p38 activation and inflammatory cytokine production, such as IL-6. Reactive Oxygen Species 52-55 NADPH oxidase 1 Homo sapiens 38-42 29269607-6 2018 This compound blocked both Nox organizer 1 (NOXO1)/Nox activator 1 (NOXA1)-dependent and phorbol 12-myristate 13-acetate-stimulated Nox1-mediated ROS production in colon cancer cells. Reactive Oxygen Species 146-149 NADPH oxidase 1 Homo sapiens 132-136 29467671-12 2018 Altogether these results suggest that Cdk5 activation is implicated in the ROS production by NOX1 and NOX2/NADPH oxidase complexes during inflammatory pain. Reactive Oxygen Species 75-78 NADPH oxidase 1 Homo sapiens 93-97 29467671-1 2018 The participation of reactive oxygen species (ROS) generated by NOX1 and NOX2/NADPH oxidase has been documented during inflammatory pain. Reactive Oxygen Species 46-49 NADPH oxidase 1 Homo sapiens 64-68 28343901-2 2018 Cardiovascular diseases are characterized by increased production of reactive oxygen species (ROS) by NAPDH oxidase 1 (Nox1) and additional Nox isoforms among other sources. Reactive Oxygen Species 69-92 NADPH oxidase 1 Homo sapiens 102-117 28343901-2 2018 Cardiovascular diseases are characterized by increased production of reactive oxygen species (ROS) by NAPDH oxidase 1 (Nox1) and additional Nox isoforms among other sources. Reactive Oxygen Species 69-92 NADPH oxidase 1 Homo sapiens 119-123 28343901-2 2018 Cardiovascular diseases are characterized by increased production of reactive oxygen species (ROS) by NAPDH oxidase 1 (Nox1) and additional Nox isoforms among other sources. Reactive Oxygen Species 94-97 NADPH oxidase 1 Homo sapiens 102-117 28343901-2 2018 Cardiovascular diseases are characterized by increased production of reactive oxygen species (ROS) by NAPDH oxidase 1 (Nox1) and additional Nox isoforms among other sources. Reactive Oxygen Species 94-97 NADPH oxidase 1 Homo sapiens 119-123 28343901-4 2018 However, GPER also has constitutive activity, e.g. in the absence of specific agonists, that was recently shown to promote hypertension and aging-induced tissue damage by promoting Nox1-derived production of ROS. Reactive Oxygen Species 208-211 NADPH oxidase 1 Homo sapiens 181-185 28510506-7 2017 The ROS sources, NOX1 and NOX4, increase biglycan-induced inflammation, while NOX2 is a negative regulator. Reactive Oxygen Species 4-7 NADPH oxidase 1 Homo sapiens 17-21 28363602-10 2017 Nox1 upregulation was inhibited by actinomycin D (ACD), an inhibitor of transcription, by inhibition of NF-kappaB, a known Nox1 transcriptional regulator and by N-acetyl cysteine (NAC) and MitoTEMPO, suggesting that NF-kappaB and mitochondrial ROS mediate zinc effects. Reactive Oxygen Species 244-247 NADPH oxidase 1 Homo sapiens 0-4 29042481-6 2017 At the molecular level, TSP1 increased Nox1-dependent generation of reactive oxygen species (ROS), leading to the increased abundance of the transcription factor p53. Reactive Oxygen Species 68-91 NADPH oxidase 1 Homo sapiens 39-43 29042481-6 2017 At the molecular level, TSP1 increased Nox1-dependent generation of reactive oxygen species (ROS), leading to the increased abundance of the transcription factor p53. Reactive Oxygen Species 93-96 NADPH oxidase 1 Homo sapiens 39-43 29042481-10 2017 Conversely, lung tissue from aging humans displayed increases in the abundance of vascular TSP1, Nox1, p53, and p21cip Finally, genetic ablation or pharmacological blockade of Nox1 in human endothelial cells attenuated TSP1-mediated ROS generation, restored cell cycle progression, and protected against senescence. Reactive Oxygen Species 233-236 NADPH oxidase 1 Homo sapiens 176-180 29262595-2 2017 Our previous work has shown that oxaliplatin efficacy depends on the reactive oxygen species (ROS) produced by Nox1. Reactive Oxygen Species 69-92 NADPH oxidase 1 Homo sapiens 111-115 29262595-2 2017 Our previous work has shown that oxaliplatin efficacy depends on the reactive oxygen species (ROS) produced by Nox1. Reactive Oxygen Species 94-97 NADPH oxidase 1 Homo sapiens 111-115 29262595-4 2017 Our results show that basal ROS production by Nox1 is increased in resistant cells. Reactive Oxygen Species 28-31 NADPH oxidase 1 Homo sapiens 46-50 29262595-7 2017 In sensitive cells, calpains inhibit Nox1 by cleaving NoxA1 leading to a transient ROS production necessary for oxaliplatin cytotoxic effects. Reactive Oxygen Species 83-86 NADPH oxidase 1 Homo sapiens 37-41 29262595-8 2017 In contrast, in resistant cells calpain activation is associated with an increase of Nox1 activity through Src kinases, inducing a strong and maintained ROS production responsible for cell survival. Reactive Oxygen Species 153-156 NADPH oxidase 1 Homo sapiens 85-89 28855537-6 2017 We specifically identified NOX1 and NOX2 enzymes to be responsible for ROS generation. Reactive Oxygen Species 71-74 NADPH oxidase 1 Homo sapiens 27-31 28855537-7 2017 Inhibition of NOX2 and NOX1 with siRNA or chemical inhibitors significantly suppresses ROS production and DNA damage induced by BA/A. Reactive Oxygen Species 87-90 NADPH oxidase 1 Homo sapiens 23-27 28625920-1 2017 NOX1 (NADPH oxidase) similar to phagocyte NADPH oxidase, is expressed mainly in the colon epithelium and it is responsible for host defense against microbial infections by generating ROS (reactive oxygen species). Reactive Oxygen Species 183-186 NADPH oxidase 1 Homo sapiens 0-4 28625920-1 2017 NOX1 (NADPH oxidase) similar to phagocyte NADPH oxidase, is expressed mainly in the colon epithelium and it is responsible for host defense against microbial infections by generating ROS (reactive oxygen species). Reactive Oxygen Species 188-211 NADPH oxidase 1 Homo sapiens 0-4 28600286-4 2017 Moreover, we demonstrated that MyD88 lies upstream of the BLT2 ligand-BLT2 axis and that this MyD88-BLT2 cascade leads to the generation of reactive oxygen species through NADPH oxidase 1 and the subsequent activation of NF-kappaB, thereby mediating IL-13 synthesis. Reactive Oxygen Species 140-163 NADPH oxidase 1 Homo sapiens 172-187 28473438-11 2017 CONCLUSIONS: Serotonin can induce cellular Src-related kinase-regulated Nox1-induced ROS and Nrf-2 dysregulation, contributing to increased post-translational oxidative modification of proteins and activation of redox-sensitive signaling pathways in hPASMCs, associated with mitogenic responses. Reactive Oxygen Species 85-88 NADPH oxidase 1 Homo sapiens 72-76 28363602-0 2017 Zinc regulates Nox1 expression through a NF-kappaB and mitochondrial ROS dependent mechanism to induce senescence of vascular smooth muscle cells. Reactive Oxygen Species 69-72 NADPH oxidase 1 Homo sapiens 15-19 28363602-14 2017 INNOVATION AND CONCLUSION: Our data demonstrate that altered zinc distribution leading to accumulation of zinc in the mitochondria increases mitochondrial ROS production causing NF-kappaB activation which in turn upregulates Nox1 expression inducing senescence of VSMCs. Reactive Oxygen Species 155-158 NADPH oxidase 1 Homo sapiens 225-229 28232183-4 2017 Plasmid driven elevation of NOX-1 resulted in elevated ROS, loss of glucose-stimulated-insulin-secretion and increased apoptosis. Reactive Oxygen Species 55-58 NADPH oxidase 1 Homo sapiens 28-33 28969026-0 2017 Increasing UCP2 expression and decreasing NOX1/4 expression maintain chondrocyte phenotype by reducing reactive oxygen species production. Reactive Oxygen Species 103-126 NADPH oxidase 1 Homo sapiens 42-46 28969026-1 2017 The aim of this study is to demonstrate that improving the mitochondrial function can inhibite the loss of chondrocyte phenotype by regulating the expression of uncoupling protein 2(UCP2) and NADPH oxidase1/4(NOX1/4) to reduce the production of reactive oxygen species(ROS). Reactive Oxygen Species 245-268 NADPH oxidase 1 Homo sapiens 192-206 28969026-1 2017 The aim of this study is to demonstrate that improving the mitochondrial function can inhibite the loss of chondrocyte phenotype by regulating the expression of uncoupling protein 2(UCP2) and NADPH oxidase1/4(NOX1/4) to reduce the production of reactive oxygen species(ROS). Reactive Oxygen Species 245-268 NADPH oxidase 1 Homo sapiens 209-215 28969026-1 2017 The aim of this study is to demonstrate that improving the mitochondrial function can inhibite the loss of chondrocyte phenotype by regulating the expression of uncoupling protein 2(UCP2) and NADPH oxidase1/4(NOX1/4) to reduce the production of reactive oxygen species(ROS). Reactive Oxygen Species 269-272 NADPH oxidase 1 Homo sapiens 192-206 28969026-1 2017 The aim of this study is to demonstrate that improving the mitochondrial function can inhibite the loss of chondrocyte phenotype by regulating the expression of uncoupling protein 2(UCP2) and NADPH oxidase1/4(NOX1/4) to reduce the production of reactive oxygen species(ROS). Reactive Oxygen Species 269-272 NADPH oxidase 1 Homo sapiens 209-215 28969026-7 2017 Increasing and decreasing UCP2 and NOX1/4 expression, respectively, helps maintain the chondrocyte phenotype and improve mitochondrial functioning by reducing reactive oxygen species production. Reactive Oxygen Species 159-182 NADPH oxidase 1 Homo sapiens 35-39 28330872-0 2017 NADPH oxidase 1 supports proliferation of colon cancer cells by modulating reactive oxygen species-dependent signal transduction. Reactive Oxygen Species 75-98 NADPH oxidase 1 Homo sapiens 0-15 28330872-4 2017 The 80-90% decrease in NOX1 expression achieved by RNAi produced a significant decline in ROS production and a G1/S block that translated into a 2-3-fold increase in tumor cell doubling time without increased apoptosis. Reactive Oxygen Species 90-93 NADPH oxidase 1 Homo sapiens 23-27 28498822-2 2017 It has been suggested that reactive oxygen species [ROS] derived from NOX1 contribute to DNA damage and neoplastic transformation in the colon, particularly during chronic inflammatory stress. Reactive Oxygen Species 27-50 NADPH oxidase 1 Homo sapiens 70-74 28498822-2 2017 It has been suggested that reactive oxygen species [ROS] derived from NOX1 contribute to DNA damage and neoplastic transformation in the colon, particularly during chronic inflammatory stress. Reactive Oxygen Species 52-55 NADPH oxidase 1 Homo sapiens 70-74 28498822-6 2017 Increased NOX1 transcription following IL-4/IL-13 exposure was mediated by JAK1/STAT6 signaling, was associated with a ROS-related inhibition of protein tyrosine phosphatase activity, and was dependent upon activation and specific binding of GATA3 to the NOX1 promoter. Reactive Oxygen Species 119-122 NADPH oxidase 1 Homo sapiens 10-14 28498822-7 2017 NOX1-mediated ROS production increased cell cycle progression through S-phase leading to a significant increase in cellular proliferation. Reactive Oxygen Species 14-17 NADPH oxidase 1 Homo sapiens 0-4 27989756-4 2017 Whereas the bacterial-induced production of ROS in phagocytes in response to ligand binding to Formyl Peptide Receptors (FPRs) and ensuing activation of NADPH oxidase 2 (Nox2) is a well-defined mechanism, ROS generated by other cell types such as intestinal epithelia in response to microbial signals via FPRs and the NADPH oxidase 1 (Nox1) is less appreciated. Reactive Oxygen Species 44-47 NADPH oxidase 1 Homo sapiens 318-333 27989756-4 2017 Whereas the bacterial-induced production of ROS in phagocytes in response to ligand binding to Formyl Peptide Receptors (FPRs) and ensuing activation of NADPH oxidase 2 (Nox2) is a well-defined mechanism, ROS generated by other cell types such as intestinal epithelia in response to microbial signals via FPRs and the NADPH oxidase 1 (Nox1) is less appreciated. Reactive Oxygen Species 44-47 NADPH oxidase 1 Homo sapiens 335-339 27989756-4 2017 Whereas the bacterial-induced production of ROS in phagocytes in response to ligand binding to Formyl Peptide Receptors (FPRs) and ensuing activation of NADPH oxidase 2 (Nox2) is a well-defined mechanism, ROS generated by other cell types such as intestinal epithelia in response to microbial signals via FPRs and the NADPH oxidase 1 (Nox1) is less appreciated. Reactive Oxygen Species 205-208 NADPH oxidase 1 Homo sapiens 318-333 27989756-4 2017 Whereas the bacterial-induced production of ROS in phagocytes in response to ligand binding to Formyl Peptide Receptors (FPRs) and ensuing activation of NADPH oxidase 2 (Nox2) is a well-defined mechanism, ROS generated by other cell types such as intestinal epithelia in response to microbial signals via FPRs and the NADPH oxidase 1 (Nox1) is less appreciated. Reactive Oxygen Species 205-208 NADPH oxidase 1 Homo sapiens 335-339 27418140-9 2016 Taken in conjunction, these data indicate that the anti-proliferative and pro-apoptotic effect of cambogin is mediated via inducing NOX1-dependent ROS production and the dissociation of ASK1 and Trx1. Reactive Oxygen Species 147-150 NADPH oxidase 1 Homo sapiens 132-136 27743884-4 2017 Here, after peptides screening on Nox1-dependent NADPH oxidase assay in HT-29 cells, we identify a peptide (referred to as NF02), cell-active, that potently block Nox1-dependent reactive oxygen species generation. Reactive Oxygen Species 178-201 NADPH oxidase 1 Homo sapiens 34-38 27743884-4 2017 Here, after peptides screening on Nox1-dependent NADPH oxidase assay in HT-29 cells, we identify a peptide (referred to as NF02), cell-active, that potently block Nox1-dependent reactive oxygen species generation. Reactive Oxygen Species 178-201 NADPH oxidase 1 Homo sapiens 163-167 27743884-6 2017 NF02 was not cytotoxic, inhibited reactive oxygen species production of reconstituted Nox1/Noxo1/Noxa1 complex in HEK293 and did not decrease Nox2 dependent cellular NADPH oxidase reactive oxygen species production. Reactive Oxygen Species 34-57 NADPH oxidase 1 Homo sapiens 86-90 27773825-3 2016 The major and more specific source of ROS in the cardiovascular system is the NADPH oxidase (NOX) family of enzymes composed of seven members (NOX1-5, DUOX 1/2). Reactive Oxygen Species 38-41 NADPH oxidase 1 Homo sapiens 143-149 27381955-0 2016 Reactive oxygen species derived from NADPH oxidase 1 and mitochondria mediate angiotensin II-induced smooth muscle cell senescence. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 37-52 27381955-8 2016 Nox1 siRNA inhibited both early and sustained ROS increases induced by Ang II. Reactive Oxygen Species 46-49 NADPH oxidase 1 Homo sapiens 0-4 26678171-4 2016 Enhanced expression and activity of Nox1 under pathologic conditions results in excessive production of reactive oxygen species and dysregulated cellular function. Reactive Oxygen Species 104-127 NADPH oxidase 1 Homo sapiens 36-40 27107996-5 2016 Using CRC cell lines expressing exogenous c-myb we show that c-Myb protects CRC cells from the cisplatin-, oxaliplatin-, and doxorubicin-induced apoptosis, elevates reactive oxygen species via up-regulation of NOX1, and sustains the pro-survival p38 MAPK pathway. Reactive Oxygen Species 165-188 NADPH oxidase 1 Homo sapiens 210-214 27094494-1 2016 Nox1 is an abundant source of reactive oxygen species (ROS) in colon epithelium recently shown to function in wound healing and epithelial homeostasis. Reactive Oxygen Species 30-53 NADPH oxidase 1 Homo sapiens 0-4 27094494-1 2016 Nox1 is an abundant source of reactive oxygen species (ROS) in colon epithelium recently shown to function in wound healing and epithelial homeostasis. Reactive Oxygen Species 55-58 NADPH oxidase 1 Homo sapiens 0-4 26815118-8 2016 Production of ROS was inhibited by both the NADPH oxidase 1 (NOX1) inhibitor STK301831 and NOX1 knock-down, which also impaired TACE/ADAM17 activation and thus EGFR phosphorylation. Reactive Oxygen Species 14-17 NADPH oxidase 1 Homo sapiens 44-59 26815118-8 2016 Production of ROS was inhibited by both the NADPH oxidase 1 (NOX1) inhibitor STK301831 and NOX1 knock-down, which also impaired TACE/ADAM17 activation and thus EGFR phosphorylation. Reactive Oxygen Species 14-17 NADPH oxidase 1 Homo sapiens 61-65 26815118-8 2016 Production of ROS was inhibited by both the NADPH oxidase 1 (NOX1) inhibitor STK301831 and NOX1 knock-down, which also impaired TACE/ADAM17 activation and thus EGFR phosphorylation. Reactive Oxygen Species 14-17 NADPH oxidase 1 Homo sapiens 91-95 26815118-11 2016 In conclusion, CAV1 is required for TGF-beta-mediated activation of TACE/ADAM17 through a mechanism that involves phosphorylation of Src and NOX1-mediated ROS production. Reactive Oxygen Species 155-158 NADPH oxidase 1 Homo sapiens 141-145 26781991-9 2016 Taken together, these results support a model whereby Nox1 activity and ROS generation are regulated by Grb2/Cbl-mediated proteolysis of NoxO1 in response to EGF, providing new insight into the processes by which excessive ROS production may promote oncogenic signaling to drive colorectal tumorigenesis. Reactive Oxygen Species 223-226 NADPH oxidase 1 Homo sapiens 54-58 26682942-1 2016 OBJECTIVE: NOX-1 and NOX-4 are key enzymes responsible for reactive oxygen species (ROS) generation in vascular smooth muscle cells (VSMC). Reactive Oxygen Species 59-82 NADPH oxidase 1 Homo sapiens 11-16 26682942-1 2016 OBJECTIVE: NOX-1 and NOX-4 are key enzymes responsible for reactive oxygen species (ROS) generation in vascular smooth muscle cells (VSMC). Reactive Oxygen Species 84-87 NADPH oxidase 1 Homo sapiens 11-16 27200149-5 2016 Instead, we found that NS5A contributes to ROS production by activating expression of NADPH oxidases 1 and 4 as well as cytochrome P450 2E1. Reactive Oxygen Species 43-46 NADPH oxidase 1 Homo sapiens 86-108 25378528-0 2014 NOXious phosphorylation: Smooth muscle reactive oxygen species production is facilitated by direct activation of the NADPH oxidase Nox1. Reactive Oxygen Species 39-62 NADPH oxidase 1 Homo sapiens 131-135 27313830-7 2016 eMPs contained Nox1, Nox2, Nox4, p47(phox), p67(phox), and p22(phox) and they produced ROS which was inhibited by the Nox inhibitor, apocynin. Reactive Oxygen Species 87-90 NADPH oxidase 1 Homo sapiens 15-19 26545779-1 2015 NADPH oxidase 1 (NOX1) plays a key role in tumorigenesis and metastasis through generating reactive oxygen species (ROS), an important intracellular signaling molecule. Reactive Oxygen Species 91-114 NADPH oxidase 1 Homo sapiens 0-15 26545779-1 2015 NADPH oxidase 1 (NOX1) plays a key role in tumorigenesis and metastasis through generating reactive oxygen species (ROS), an important intracellular signaling molecule. Reactive Oxygen Species 91-114 NADPH oxidase 1 Homo sapiens 17-21 26545779-1 2015 NADPH oxidase 1 (NOX1) plays a key role in tumorigenesis and metastasis through generating reactive oxygen species (ROS), an important intracellular signaling molecule. Reactive Oxygen Species 116-119 NADPH oxidase 1 Homo sapiens 0-15 26545779-1 2015 NADPH oxidase 1 (NOX1) plays a key role in tumorigenesis and metastasis through generating reactive oxygen species (ROS), an important intracellular signaling molecule. Reactive Oxygen Species 116-119 NADPH oxidase 1 Homo sapiens 17-21 26545779-5 2015 Further study into the mechanism we found that increased NOX1 expression elevated intracellular ROS levels, which then activated HIF-1alpha/MDR1 pathway. Reactive Oxygen Species 96-99 NADPH oxidase 1 Homo sapiens 57-61 26520903-5 2015 Ang II also stimulates ROS production in VSMC (140%) that is NOX1 dependent, being completely inhibited in NOX1 silenced cells. Reactive Oxygen Species 23-26 NADPH oxidase 1 Homo sapiens 61-65 26520903-5 2015 Ang II also stimulates ROS production in VSMC (140%) that is NOX1 dependent, being completely inhibited in NOX1 silenced cells. Reactive Oxygen Species 23-26 NADPH oxidase 1 Homo sapiens 107-111 26301257-9 2015 All NOX1 and DUOX2 variants showed reduced ROS production compared with wild-type enzymes. Reactive Oxygen Species 43-46 NADPH oxidase 1 Homo sapiens 4-8 26116564-13 2015 CONCLUSIONS: Molecular switch from NOX1 to NOX2 in colon cancer cells induces ROS production and subsequently enhances MMP-7 expression by deactivating AMPK, which otherwise inhibits stimulus-induced autoregulation of ROS and NOX2 gene expression. Reactive Oxygen Species 78-81 NADPH oxidase 1 Homo sapiens 35-39 26116564-13 2015 CONCLUSIONS: Molecular switch from NOX1 to NOX2 in colon cancer cells induces ROS production and subsequently enhances MMP-7 expression by deactivating AMPK, which otherwise inhibits stimulus-induced autoregulation of ROS and NOX2 gene expression. Reactive Oxygen Species 218-221 NADPH oxidase 1 Homo sapiens 35-39 25592377-0 2015 NADPH oxidase 1-dependent ROS is crucial for TLR4 signaling to promote tumor metastasis of non-small cell lung cancer. Reactive Oxygen Species 26-29 NADPH oxidase 1 Homo sapiens 0-15 25592377-13 2015 Our findings demonstrated a crucial role of NOX1-dependent ROS for TLR4 signaling to enhance the metastasis of NSCLC, which could further the understanding of NSCLC pathogenesis and helpful for developing novel therapeutics for NSCLC. Reactive Oxygen Species 59-62 NADPH oxidase 1 Homo sapiens 44-48 25550204-4 2015 This study was designed to test the hypothesis that pathological CS stimulates NADPH oxidase isoform 1 (Nox1)-derived ROS via MEF2B, leading to VSMC dysfunction via a switch from a contractile to a synthetic phenotype. Reactive Oxygen Species 118-121 NADPH oxidase 1 Homo sapiens 79-102 25550204-4 2015 This study was designed to test the hypothesis that pathological CS stimulates NADPH oxidase isoform 1 (Nox1)-derived ROS via MEF2B, leading to VSMC dysfunction via a switch from a contractile to a synthetic phenotype. Reactive Oxygen Species 118-121 NADPH oxidase 1 Homo sapiens 104-108 25550204-5 2015 APPROACH AND RESULTS: Using a newly developed isoform-specific Nox1 inhibitor and gene silencing technology, we demonstrate that a novel pathway, including MEF2B-Nox1-ROS, is upregulated under pathological stretch conditions, and this pathway promotes a VSMC phenotypic switch from a contractile to a synthetic phenotype. Reactive Oxygen Species 167-170 NADPH oxidase 1 Homo sapiens 63-67 25550204-5 2015 APPROACH AND RESULTS: Using a newly developed isoform-specific Nox1 inhibitor and gene silencing technology, we demonstrate that a novel pathway, including MEF2B-Nox1-ROS, is upregulated under pathological stretch conditions, and this pathway promotes a VSMC phenotypic switch from a contractile to a synthetic phenotype. Reactive Oxygen Species 167-170 NADPH oxidase 1 Homo sapiens 162-166 25550204-7 2015 Furthermore, we show that stretch-induced Nox1-derived ROS upregulated a specific marker for synthetic phenotype (osteopontin), whereas it downregulated classical markers for contractile phenotype (calponin1 and smoothelin B). Reactive Oxygen Species 55-58 NADPH oxidase 1 Homo sapiens 42-46 25550204-9 2015 CONCLUSIONS: These results suggest that CS initiates a signal through MEF2B that potentiates Nox1-mediated ROS production and causes VSMC to switch to a synthetic phenotype. Reactive Oxygen Species 107-110 NADPH oxidase 1 Homo sapiens 93-97 25228390-8 2014 Moreover, Nox1 threonine 429 phosphorylation facilitated the association of Nox1 with the NoxA1 activation domain and was necessary for NADPH oxidase complex assembly, reactive oxygen species production, and vascular smooth muscle cell migration. Reactive Oxygen Species 168-191 NADPH oxidase 1 Homo sapiens 10-14 25228390-8 2014 Moreover, Nox1 threonine 429 phosphorylation facilitated the association of Nox1 with the NoxA1 activation domain and was necessary for NADPH oxidase complex assembly, reactive oxygen species production, and vascular smooth muscle cell migration. Reactive Oxygen Species 168-191 NADPH oxidase 1 Homo sapiens 76-80 26184677-6 2015 CCL11 significantly promoted the migration of microglia, and induced microglial production of reactive oxygen species by upregulating nicotinamide adenine dinucleotide phosphate-oxidase 1 (NOX1), thereby promoting excitotoxic neuronal death. Reactive Oxygen Species 94-117 NADPH oxidase 1 Homo sapiens 134-187 26184677-6 2015 CCL11 significantly promoted the migration of microglia, and induced microglial production of reactive oxygen species by upregulating nicotinamide adenine dinucleotide phosphate-oxidase 1 (NOX1), thereby promoting excitotoxic neuronal death. Reactive Oxygen Species 94-117 NADPH oxidase 1 Homo sapiens 189-193 26442864-6 2015 Additionally, NRROS attenuates RANKL-induced NF-N:B activation, as well as degradation of the NOX1 and NOX2 proteins, which are required for ROS generation. Reactive Oxygen Species 16-19 NADPH oxidase 1 Homo sapiens 94-98 25818486-3 2015 Recent evidence suggests that both NOX1 and DUOX2 species produce ROS in the gastrointestinal tract as a result of chronic inflammatory stress; cytokine induction (by interferon-gamma, tumour necrosis factor alpha, and interleukins IL-4 and IL-13) of NOX1 and DUOX2 may contribute to the development of colorectal and pancreatic carcinomas in patients with inflammatory bowel disease and chronic pancreatitis, respectively. Reactive Oxygen Species 66-69 NADPH oxidase 1 Homo sapiens 35-39 25806803-2 2015 The NOX1 subunit is over-expressed in several cancers and NOX1 derived ROS have been repeatedly linked with tumorigenesis and tumor progression although underlying pathways are ill defined. Reactive Oxygen Species 71-74 NADPH oxidase 1 Homo sapiens 4-8 25806803-2 2015 The NOX1 subunit is over-expressed in several cancers and NOX1 derived ROS have been repeatedly linked with tumorigenesis and tumor progression although underlying pathways are ill defined. Reactive Oxygen Species 71-74 NADPH oxidase 1 Homo sapiens 58-62 25540919-4 2015 RSV exhibits a strong ability to inhibit high glucose-induced EMT by decreasing intracellular ROS levels via down-regulation of NADPH oxidase subunits NOX1 and NOX4. Reactive Oxygen Species 94-97 NADPH oxidase 1 Homo sapiens 151-155 25871260-3 2015 METHODS: Three ROS-related enzymes-nicotinamide adenine dinucleotide phosphate oxidase (NOX)-1 and -2 and catalase-were investigated in interface membrane tissues and in titanium (Ti) particle-stimulated macrophages in vitro. Reactive Oxygen Species 15-18 NADPH oxidase 1 Homo sapiens 35-101 25871260-6 2015 NOX-1 and -2 were highly expressed in aseptically loosened interface membranes and in macrophages stimulated with Ti particles; the particles induced a moderate amount of ROS generation, NF-kappaB activation, and TNF-alpha secretion in macrophages, and these effects were suppressed by apocynin. Reactive Oxygen Species 171-174 NADPH oxidase 1 Homo sapiens 0-12 24917593-4 2014 Memo was also required for the sustained production of the ROS O2- by NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase 1 (NOX1) in breast cancer cells. Reactive Oxygen Species 59-62 NADPH oxidase 1 Homo sapiens 149-153 24632950-3 2014 In the present study, we found that oncogenic K-Ras induces ROS generation through activation of NADPH oxidase 1 (NOX1), which is a critical regulator for the K-Ras-induced cellular transformation. Reactive Oxygen Species 60-63 NADPH oxidase 1 Homo sapiens 97-112 24632950-3 2014 In the present study, we found that oncogenic K-Ras induces ROS generation through activation of NADPH oxidase 1 (NOX1), which is a critical regulator for the K-Ras-induced cellular transformation. Reactive Oxygen Species 60-63 NADPH oxidase 1 Homo sapiens 114-118 24632950-6 2014 Notably, oncogenic K-Ras activated all MAPKs (JNK, ERK and p38); however, only p38 was involved in p47(phox)-NOX1-dependent ROS generation and consequent transformation. Reactive Oxygen Species 124-127 NADPH oxidase 1 Homo sapiens 109-113 24632950-8 2014 In agreement with the mechanism, inhibition of p38, PDPK1, PKCdelta, p47(phox) or NOX1 effectively blocked K-Ras-induced ROS generation, anchorage-independent colony formation and tumor formation. Reactive Oxygen Species 121-124 NADPH oxidase 1 Homo sapiens 82-86 24632950-9 2014 Taken together, our findings demonstrated that oncogenic K-Ras activates the signaling cascade p38/PDPK1/PKCdelta/p47(phox)/NOX1 for ROS generation and consequent malignant cellular transformation. Reactive Oxygen Species 133-136 NADPH oxidase 1 Homo sapiens 124-128 24437351-0 2014 The involvement of reactive oxygen species derived from NADPH oxidase-1 activation on the constitutive tyrosine auto-phosphorylation of RET proteins. Reactive Oxygen Species 19-42 NADPH oxidase 1 Homo sapiens 56-71 24192910-5 2014 Here we report that specific members of the gut microbiota stimulate FPR1 on intestinal epithelial cells to generate reactive oxygen species via enterocyte NADPH oxidase 1 (NOX1), causing rapid phosphorylation of focal adhesion kinase (FAK) and extracellular signal-regulated kinase mitogen-activated protein kinase. Reactive Oxygen Species 117-140 NADPH oxidase 1 Homo sapiens 156-171 24192910-5 2014 Here we report that specific members of the gut microbiota stimulate FPR1 on intestinal epithelial cells to generate reactive oxygen species via enterocyte NADPH oxidase 1 (NOX1), causing rapid phosphorylation of focal adhesion kinase (FAK) and extracellular signal-regulated kinase mitogen-activated protein kinase. Reactive Oxygen Species 117-140 NADPH oxidase 1 Homo sapiens 173-177 24192910-7 2014 Taken together, these findings identify a novel role of FPR1 as pattern recognition receptors for perceiving the enteric microbiota that promotes repair of mucosal wounds via generation of reactive oxygen species from the enterocyte NOX1. Reactive Oxygen Species 189-212 NADPH oxidase 1 Homo sapiens 233-237 24437351-6 2014 Elevated ROS derived from NOX1 activation and downregulation of SOD in NIH3T3RET-MEN2A and NIH3T3RET-MEN 2B cells may be involved in RET constitutive tyrosine auto-phosphorylation, and scavengers of ROS such as catalase and blocking NOX1 are useful for targeting RET tyrosine kinase activation in cancer. Reactive Oxygen Species 9-12 NADPH oxidase 1 Homo sapiens 233-237 24637602-4 2014 Whereas NADPH oxidase 2 (Nox2) catalyzed ROS generation in response to microbial perception by bone marrow-derived phagocytes is well-studied, the function of ROS generated by Nox1 in enterocytes in response to microbial signals is not fully understood. Reactive Oxygen Species 159-162 NADPH oxidase 1 Homo sapiens 176-180 24355212-8 2014 Subsequently, mitochondria and nicotinamide adenine dinucleotide phosphate oxidase (NADPH) isoforms (Nox1 and Nox4 in colon and kidney, respectively) are activated for reactive oxygen species (ROS) production, and the resulting excess ROS can attack the DNA, causing DNA oxidation. Reactive Oxygen Species 168-191 NADPH oxidase 1 Homo sapiens 101-105 24355212-8 2014 Subsequently, mitochondria and nicotinamide adenine dinucleotide phosphate oxidase (NADPH) isoforms (Nox1 and Nox4 in colon and kidney, respectively) are activated for reactive oxygen species (ROS) production, and the resulting excess ROS can attack the DNA, causing DNA oxidation. Reactive Oxygen Species 193-196 NADPH oxidase 1 Homo sapiens 101-105 24355212-8 2014 Subsequently, mitochondria and nicotinamide adenine dinucleotide phosphate oxidase (NADPH) isoforms (Nox1 and Nox4 in colon and kidney, respectively) are activated for reactive oxygen species (ROS) production, and the resulting excess ROS can attack the DNA, causing DNA oxidation. Reactive Oxygen Species 235-238 NADPH oxidase 1 Homo sapiens 101-105 24439294-1 2014 INTRODUCTION: Nicotinamide adenine dinucleotide phosphate oxidases (NOX 1-5) are enzymes that generate cellular reactive oxygen species (ROS) besides mitochondria and might be important ROS sources associated with pregnancy complications, particularly preterm premature rupture of membranes (pPROM), that has been related to ROS. Reactive Oxygen Species 112-135 NADPH oxidase 1 Homo sapiens 68-75 24439294-1 2014 INTRODUCTION: Nicotinamide adenine dinucleotide phosphate oxidases (NOX 1-5) are enzymes that generate cellular reactive oxygen species (ROS) besides mitochondria and might be important ROS sources associated with pregnancy complications, particularly preterm premature rupture of membranes (pPROM), that has been related to ROS. Reactive Oxygen Species 137-140 NADPH oxidase 1 Homo sapiens 68-75 24439294-1 2014 INTRODUCTION: Nicotinamide adenine dinucleotide phosphate oxidases (NOX 1-5) are enzymes that generate cellular reactive oxygen species (ROS) besides mitochondria and might be important ROS sources associated with pregnancy complications, particularly preterm premature rupture of membranes (pPROM), that has been related to ROS. Reactive Oxygen Species 186-189 NADPH oxidase 1 Homo sapiens 68-75 24439294-1 2014 INTRODUCTION: Nicotinamide adenine dinucleotide phosphate oxidases (NOX 1-5) are enzymes that generate cellular reactive oxygen species (ROS) besides mitochondria and might be important ROS sources associated with pregnancy complications, particularly preterm premature rupture of membranes (pPROM), that has been related to ROS. Reactive Oxygen Species 186-189 NADPH oxidase 1 Homo sapiens 68-75 24140706-4 2014 ATG increased cellular reactive oxygen species (ROS) production by increasing p22(phox)/NADPH oxidase 1 interaction and decreasing glutathione level. Reactive Oxygen Species 23-46 NADPH oxidase 1 Homo sapiens 88-103 24140706-4 2014 ATG increased cellular reactive oxygen species (ROS) production by increasing p22(phox)/NADPH oxidase 1 interaction and decreasing glutathione level. Reactive Oxygen Species 48-51 NADPH oxidase 1 Homo sapiens 88-103 24669283-0 2014 NADPH oxidase 1 and its derived reactive oxygen species mediated tissue injury and repair. Reactive Oxygen Species 32-55 NADPH oxidase 1 Homo sapiens 0-15 23600794-4 2014 A major source for ROS in the cardiovascular-renal system is a family of nicotinamide adenine dinucleotide phosphate oxidases (Noxs), including the prototypic Nox2-based Nox, and Nox family members: Nox1, Nox4, and Nox5. Reactive Oxygen Species 19-22 NADPH oxidase 1 Homo sapiens 199-203 25215174-7 2014 These findings suggest that ROS produced by St is generated through NOX1 and NOX4. Reactive Oxygen Species 28-31 NADPH oxidase 1 Homo sapiens 68-72 24669283-6 2014 NADPH oxidase 1 and its derived reactive oxygen species are suggested to be able to regulate inflammation reaction, cell proliferation and migration, and extracellular matrix synthesis, which contribute to the processes of tissue injury and repair. Reactive Oxygen Species 32-55 NADPH oxidase 1 Homo sapiens 0-15 23937589-4 2013 While the induced production of ROS in professional phagocytes via stimulation of formyl peptide receptors (FPRs) and activation of NADPH oxidase 2 (Nox2) is a well-studied process, ROS are also similarly elicited in other cell types, including intestinal epithelia, in response to microbial signals via FPRs and the epithelial NADPH oxidase 1 (Nox1). Reactive Oxygen Species 32-35 NADPH oxidase 1 Homo sapiens 328-343 24187133-1 2013 Excessive vascular and colon epithelial reactive oxygen species production by NADPH oxidase isoform 1 (Nox1) has been implicated in a number of disease states, including hypertension, atherosclerosis, and neoplasia. Reactive Oxygen Species 40-63 NADPH oxidase 1 Homo sapiens 78-101 24187133-1 2013 Excessive vascular and colon epithelial reactive oxygen species production by NADPH oxidase isoform 1 (Nox1) has been implicated in a number of disease states, including hypertension, atherosclerosis, and neoplasia. Reactive Oxygen Species 40-63 NADPH oxidase 1 Homo sapiens 103-107 24187133-2 2013 A peptide that mimics a putative activation domain of the Nox1 activator subunit NOXA1 (NOXA1 docking sequence, also known as NoxA1ds) potently inhibited Nox1-derived superoxide anion (O2 -) production in a reconstituted Nox1 cell-free system, with no effect on Nox2-, Nox4-, Nox5-, or xanthine oxidase-derived reactive oxygen species production as measured by cytochrome c reduction, Amplex Red fluorescence, and electron paramagnetic resonance. Reactive Oxygen Species 311-334 NADPH oxidase 1 Homo sapiens 58-62 24187133-2 2013 A peptide that mimics a putative activation domain of the Nox1 activator subunit NOXA1 (NOXA1 docking sequence, also known as NoxA1ds) potently inhibited Nox1-derived superoxide anion (O2 -) production in a reconstituted Nox1 cell-free system, with no effect on Nox2-, Nox4-, Nox5-, or xanthine oxidase-derived reactive oxygen species production as measured by cytochrome c reduction, Amplex Red fluorescence, and electron paramagnetic resonance. Reactive Oxygen Species 311-334 NADPH oxidase 1 Homo sapiens 154-158 24187133-2 2013 A peptide that mimics a putative activation domain of the Nox1 activator subunit NOXA1 (NOXA1 docking sequence, also known as NoxA1ds) potently inhibited Nox1-derived superoxide anion (O2 -) production in a reconstituted Nox1 cell-free system, with no effect on Nox2-, Nox4-, Nox5-, or xanthine oxidase-derived reactive oxygen species production as measured by cytochrome c reduction, Amplex Red fluorescence, and electron paramagnetic resonance. Reactive Oxygen Species 311-334 NADPH oxidase 1 Homo sapiens 154-158 23937589-4 2013 While the induced production of ROS in professional phagocytes via stimulation of formyl peptide receptors (FPRs) and activation of NADPH oxidase 2 (Nox2) is a well-studied process, ROS are also similarly elicited in other cell types, including intestinal epithelia, in response to microbial signals via FPRs and the epithelial NADPH oxidase 1 (Nox1). Reactive Oxygen Species 32-35 NADPH oxidase 1 Homo sapiens 345-349 23583258-4 2013 This strong pro-inflammatory effect appeared to be dependent on the net imbalance of red-ox equilibrium with the production of excessive levels of reactive oxygen species through the colonic NADPH-oxidase NOX1 activation. Reactive Oxygen Species 147-170 NADPH oxidase 1 Homo sapiens 205-209 23970124-5 2013 NADPH oxidases are one of the many sources of ROS in biologic systems, and there are seven isoforms (Nox1-5, Duox1, Duox2). Reactive Oxygen Species 46-49 NADPH oxidase 1 Homo sapiens 101-107 22530599-6 2013 RECENT ADVANCES: Ang II regulates vascular cell production of ROS through various recently characterized Noxs, including Nox1, Nox2, Nox4, and Nox5. Reactive Oxygen Species 62-65 NADPH oxidase 1 Homo sapiens 121-125 23606279-6 2013 Our results showed that the interaction of activated monocytes with SMC determines: (i) phosphorylation of STAT3 and reduction of SOCS3 expression in both cell types; (ii) intracellular ROS production dependent on NADPH oxidase (by increased Nox1 expression) and STAT3 activation in SMC; (iii) up-regulation of resistin expression in monocytes dependent on STAT3 activation. Reactive Oxygen Species 186-189 NADPH oxidase 1 Homo sapiens 242-246 23606279-7 2013 Furthermore, exposure of SMC to resistin induces ROS by increasing NADPH oxidase activity and the p22phox and Nox1 expression. Reactive Oxygen Species 49-52 NADPH oxidase 1 Homo sapiens 110-114 23565109-9 2013 Second, regulation of NOX-1 in beta cells involves feed-forward control linked to elevated ROS and Src-kinase activation. Reactive Oxygen Species 91-94 NADPH oxidase 1 Homo sapiens 22-27 23564668-8 2013 Deletion of Nox1, but not Nox4, had a profound antiatherosclerotic effect correlating with reduced reactive oxygen species formation, attenuation of chemokine expression, vascular adhesion of leukocytes, macrophage infiltration, and reduced expression of proinflammatory and profibrotic markers. Reactive Oxygen Species 99-122 NADPH oxidase 1 Homo sapiens 12-16 23410839-3 2013 Regulation of NOX-1 expression in beta cells followed modulation of cellular reactive oxygen species (ROS); pro-oxidants increased NOX-1 (p<0.001) and anti-oxidants decreased NOX-1 (p<0.05). Reactive Oxygen Species 77-100 NADPH oxidase 1 Homo sapiens 14-19 23410839-3 2013 Regulation of NOX-1 expression in beta cells followed modulation of cellular reactive oxygen species (ROS); pro-oxidants increased NOX-1 (p<0.001) and anti-oxidants decreased NOX-1 (p<0.05). Reactive Oxygen Species 102-105 NADPH oxidase 1 Homo sapiens 14-19 23410839-8 2013 Collectively, these data indicate that expression of NOX-1 in beta cells is regulated in a feed-forward loop mediated by ROS and Src-kinase. Reactive Oxygen Species 121-124 NADPH oxidase 1 Homo sapiens 53-58 23497394-1 2013 BACKGROUND: Recent studies have demonstrated that the activation of NADPH oxidase 1 (Nox1) plays an important role in the control of reactive oxygen species and their involvement in vascular physiology and pathophysiology. Reactive Oxygen Species 133-156 NADPH oxidase 1 Homo sapiens 68-83 23322165-1 2013 Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 44-59 23322165-1 2013 Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 61-65 23322165-1 2013 Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Reactive Oxygen Species 25-28 NADPH oxidase 1 Homo sapiens 44-59 23322165-1 2013 Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Reactive Oxygen Species 25-28 NADPH oxidase 1 Homo sapiens 61-65 23497394-1 2013 BACKGROUND: Recent studies have demonstrated that the activation of NADPH oxidase 1 (Nox1) plays an important role in the control of reactive oxygen species and their involvement in vascular physiology and pathophysiology. Reactive Oxygen Species 133-156 NADPH oxidase 1 Homo sapiens 85-89 23092829-5 2013 The enhanced production of reactive oxygen species through up-regulation of the colonic NADPH-oxidase isoform NOX1 appeared to be the key event in oxysterol-induced apoptosis in these colon cancer cells. Reactive Oxygen Species 27-50 NADPH oxidase 1 Homo sapiens 110-114 22931418-7 2013 Cancer cells may produce high levels of ROS, and in some cases, the source of these ROS has been linked to NOX/DUOX deregulation as reported for prostate cancer (NOX1 and NOX5), melanoma and glioblastoma (NOX4) among others. Reactive Oxygen Species 40-43 NADPH oxidase 1 Homo sapiens 162-166 22931418-7 2013 Cancer cells may produce high levels of ROS, and in some cases, the source of these ROS has been linked to NOX/DUOX deregulation as reported for prostate cancer (NOX1 and NOX5), melanoma and glioblastoma (NOX4) among others. Reactive Oxygen Species 84-87 NADPH oxidase 1 Homo sapiens 162-166 23372061-6 2013 AFABP overexpression increased reactive oxygen species production by upregulating the expression of NADPH oxidase subunits Nox1, Nox4, and P22 through multiple pathways, with elevation of downstream gene cyclin D1, matrix metalloproteinase-2, and monocyte chemoattractant protein-1. Reactive Oxygen Species 31-54 NADPH oxidase 1 Homo sapiens 123-127 23223568-5 2013 Poly-Ub/BGIN interactions support BGIN-mediated inactivation of a membranous Rac1 population, which consequently inactivates membrane-localized Rac1 effector systems such as reactive oxygen species (ROS) generation by the Nox1 complex. Reactive Oxygen Species 174-197 NADPH oxidase 1 Homo sapiens 222-226 23467460-0 2013 Entamoeba histolytica induces cell death of HT29 colonic epithelial cells via NOX1-derived ROS. Reactive Oxygen Species 91-94 NADPH oxidase 1 Homo sapiens 78-82 23467460-9 2013 We next investigated whether NADPH oxidase 1 (NOX1)-derived ROS is closely associated with HT29 cell death induced by E. histolytica. Reactive Oxygen Species 60-63 NADPH oxidase 1 Homo sapiens 29-44 23467460-9 2013 We next investigated whether NADPH oxidase 1 (NOX1)-derived ROS is closely associated with HT29 cell death induced by E. histolytica. Reactive Oxygen Species 60-63 NADPH oxidase 1 Homo sapiens 46-50 23467460-12 2013 These results suggest that NOX1-derived ROS is required for apoptotic cell death in HT29 colon epithelial cells induced by E. histolytica. Reactive Oxygen Species 40-43 NADPH oxidase 1 Homo sapiens 27-31 23223568-5 2013 Poly-Ub/BGIN interactions support BGIN-mediated inactivation of a membranous Rac1 population, which consequently inactivates membrane-localized Rac1 effector systems such as reactive oxygen species (ROS) generation by the Nox1 complex. Reactive Oxygen Species 199-202 NADPH oxidase 1 Homo sapiens 222-226 22503554-2 2012 NOX1, NOX2, and NOX4 are important sources of reactive oxygen species in the heart, but knowledge of the calcium-dependent NOX5 in the heart is lacking. Reactive Oxygen Species 46-69 NADPH oxidase 1 Homo sapiens 0-4 23216904-9 2013 Together, these findings suggest that Nox1- and Nox4-generated ROS play an important role in Ras-induced premature senescence, which may involve DNA damage response and p38MAPK signaling pathways. Reactive Oxygen Species 63-66 NADPH oxidase 1 Homo sapiens 38-42 23087362-8 2012 CONCLUSIONS: Our data suggest a highly regulated process of reactive oxygen species stimulation and blood flow regulation promoted through a direct TSP1/CD47-mediated activation of Nox1. Reactive Oxygen Species 60-83 NADPH oxidase 1 Homo sapiens 181-185 22773830-5 2012 We show here that platelet-derived growth factor (PDGF) promoted subcellular redistribution of PDI concomitant to Nox1-dependent reactive oxygen species production and that siRNA-mediated PDI silencing inhibited such reactive oxygen species production, while nearly totally suppressing the increase in Nox1 expression, with no change in Nox4. Reactive Oxygen Species 129-152 NADPH oxidase 1 Homo sapiens 114-118 22773830-5 2012 We show here that platelet-derived growth factor (PDGF) promoted subcellular redistribution of PDI concomitant to Nox1-dependent reactive oxygen species production and that siRNA-mediated PDI silencing inhibited such reactive oxygen species production, while nearly totally suppressing the increase in Nox1 expression, with no change in Nox4. Reactive Oxygen Species 217-240 NADPH oxidase 1 Homo sapiens 302-306 23216904-0 2013 ROS-generating oxidases Nox1 and Nox4 contribute to oncogenic Ras-induced premature senescence. Reactive Oxygen Species 0-3 NADPH oxidase 1 Homo sapiens 24-28 22502743-5 2012 Inhibitors of NADPH oxidase, apocynin and diphenyleneiodonium, and a dual selective NOX1/4 inhibitor, blocked ROS generation (p<0.01) and induction of MCP-1 (p<0.05) by pro-inflammatory cytokines in beta cells. Reactive Oxygen Species 110-113 NADPH oxidase 1 Homo sapiens 84-90 22547655-10 2012 Finally, higher expression of Nox1 and Noxo1 was found in the inflammatory region of human atherosclerotic plaques, colocalizing with VSMCs, macrophages, and ROS-producing cells. Reactive Oxygen Species 158-161 NADPH oxidase 1 Homo sapiens 30-34 22467573-9 2012 It was observed that the nonselective NAD(P)H oxidase inhibitors VAS-2870, AEBSF, and the Nox1 NAD(P)H oxidase-specific inhibitor ML-090 decreased the ROS burst stimulated by OGD, which was associated with a decreased level of RGC death. Reactive Oxygen Species 151-154 NADPH oxidase 1 Homo sapiens 90-94 22713144-4 2012 A major source for cardiovascular ROS is a family of non-phagocytic NADPH oxidases (Nox1, Nox2, Nox4, Nox5). Reactive Oxygen Species 34-37 NADPH oxidase 1 Homo sapiens 84-88 22467573-11 2012 Importantly, high levels of Nox1 NAD(P)H oxidase subunits in RGCs suggest that this enzyme could be a major source of ROS in RGCs produced by NAD(P)H oxidases. Reactive Oxygen Species 118-121 NADPH oxidase 1 Homo sapiens 28-32 23071493-6 2012 This increase in LPS-induced ROS activity is completely abrogated by a Nox inhibitor, diphenyleneiodonium (DPI), Nox1 siRNA and an NF-kappaB inhibitor, Dihydrochloride. Reactive Oxygen Species 29-32 NADPH oxidase 1 Homo sapiens 113-117 22158615-0 2012 Death receptors 4 and 5 activate Nox1 NADPH oxidase through riboflavin kinase to induce reactive oxygen species-mediated apoptotic cell death. Reactive Oxygen Species 88-111 NADPH oxidase 1 Homo sapiens 33-37 22158615-2 2012 Here we report that stimulation of DR4 and/or DR5 by the agonistic protein KD548-Fc, an Fc-fused DR4/DR5 dual-specific Kringle domain variant, activates plasma membrane-associated Nox1 NADPH oxidase to generate superoxide anion and subsequently accumulates intracellular reactive oxygen species (ROS), leading to sustained c-Jun N-terminal kinase activation and eventual apoptotic cell death in human HeLa and Jurkat tumor cells. Reactive Oxygen Species 271-294 NADPH oxidase 1 Homo sapiens 180-184 22158615-2 2012 Here we report that stimulation of DR4 and/or DR5 by the agonistic protein KD548-Fc, an Fc-fused DR4/DR5 dual-specific Kringle domain variant, activates plasma membrane-associated Nox1 NADPH oxidase to generate superoxide anion and subsequently accumulates intracellular reactive oxygen species (ROS), leading to sustained c-Jun N-terminal kinase activation and eventual apoptotic cell death in human HeLa and Jurkat tumor cells. Reactive Oxygen Species 296-299 NADPH oxidase 1 Homo sapiens 180-184 22158615-7 2012 Our results suggest that DR4 and DR5 have a capability to activate Nox1 by recruiting RFK, resulting in ROS-mediated apoptotic cell death in tumor cells. Reactive Oxygen Species 104-107 NADPH oxidase 1 Homo sapiens 67-71 22237206-0 2012 DNA damage induces reactive oxygen species generation through the H2AX-Nox1/Rac1 pathway. Reactive Oxygen Species 19-42 NADPH oxidase 1 Homo sapiens 71-75 22237206-3 2012 Increased levels of ROS and cell death induced by H2AX overexpression alone or DNA damage leading to H2AX accumulation are reduced by treating cells with the antioxidant N-Acetyl-L-Cysteine (NAC), the NADP(H) oxidase (Nox) inhibitor DPI, expression of Rac1N17, and knockdown of Nox1, but not Nox4, indicating that induction of ROS by H2AX is mediated through Nox1 and Rac1 GTPase. Reactive Oxygen Species 20-23 NADPH oxidase 1 Homo sapiens 278-282 22237206-3 2012 Increased levels of ROS and cell death induced by H2AX overexpression alone or DNA damage leading to H2AX accumulation are reduced by treating cells with the antioxidant N-Acetyl-L-Cysteine (NAC), the NADP(H) oxidase (Nox) inhibitor DPI, expression of Rac1N17, and knockdown of Nox1, but not Nox4, indicating that induction of ROS by H2AX is mediated through Nox1 and Rac1 GTPase. Reactive Oxygen Species 20-23 NADPH oxidase 1 Homo sapiens 359-363 22237206-3 2012 Increased levels of ROS and cell death induced by H2AX overexpression alone or DNA damage leading to H2AX accumulation are reduced by treating cells with the antioxidant N-Acetyl-L-Cysteine (NAC), the NADP(H) oxidase (Nox) inhibitor DPI, expression of Rac1N17, and knockdown of Nox1, but not Nox4, indicating that induction of ROS by H2AX is mediated through Nox1 and Rac1 GTPase. Reactive Oxygen Species 327-330 NADPH oxidase 1 Homo sapiens 278-282 22237206-3 2012 Increased levels of ROS and cell death induced by H2AX overexpression alone or DNA damage leading to H2AX accumulation are reduced by treating cells with the antioxidant N-Acetyl-L-Cysteine (NAC), the NADP(H) oxidase (Nox) inhibitor DPI, expression of Rac1N17, and knockdown of Nox1, but not Nox4, indicating that induction of ROS by H2AX is mediated through Nox1 and Rac1 GTPase. Reactive Oxygen Species 327-330 NADPH oxidase 1 Homo sapiens 359-363 22237206-5 2012 These results point to a novel role of histone H2AX that regulates Nox1-mediated ROS generation after DNA damage. Reactive Oxygen Species 81-84 NADPH oxidase 1 Homo sapiens 67-71 21883939-5 2012 A critical source of endothelial ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, including the prototypic Nox2-based NADPH oxidases, Nox1, Nox4 and Nox5. Reactive Oxygen Species 33-36 NADPH oxidase 1 Homo sapiens 181-185 22305747-8 2012 Exposure of HT-29 colon cancer cells, which express Nox1, to DPI and DTI confirmed their inhibitory effects on steady state ROS levels, and demonstrated decreased Stat, Erk1/2, and Akt signaling mediated by IL-4, IL-6, IL-13, and IL-22, possibly due to a concomitant increase in tumor cell phosphatase activity. Reactive Oxygen Species 124-127 NADPH oxidase 1 Homo sapiens 52-56 22445098-5 2012 A major source for cardiovascular ROS is a family of nonphagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox1, Nox2, Nox4, and Nox5). Reactive Oxygen Species 34-37 NADPH oxidase 1 Homo sapiens 129-133 22342885-1 2012 NOXO1beta [NOXO1 (Nox organizer 1) beta] is a cytosolic protein that, in conjunction with NOXA1 (Nox activator 1), regulates generation of reactive oxygen species by the NADPH oxidase 1 (Nox1) enzyme complex. Reactive Oxygen Species 139-162 NADPH oxidase 1 Homo sapiens 170-185 22342885-1 2012 NOXO1beta [NOXO1 (Nox organizer 1) beta] is a cytosolic protein that, in conjunction with NOXA1 (Nox activator 1), regulates generation of reactive oxygen species by the NADPH oxidase 1 (Nox1) enzyme complex. Reactive Oxygen Species 139-162 NADPH oxidase 1 Homo sapiens 187-191 22120521-1 2012 NADPH oxidase 1 (Nox1) is essential for reactive oxygen species production in the innate immune responses mediated by toll-like receptor (TLR), but the mechanism regulating its expression remains uncertain. Reactive Oxygen Species 40-63 NADPH oxidase 1 Homo sapiens 0-15 22120521-1 2012 NADPH oxidase 1 (Nox1) is essential for reactive oxygen species production in the innate immune responses mediated by toll-like receptor (TLR), but the mechanism regulating its expression remains uncertain. Reactive Oxygen Species 40-63 NADPH oxidase 1 Homo sapiens 17-21 22071588-5 2012 In vascular cells, the NADPH oxidase isoforms Nox1, Nox2, Nox4, and Nox5 are expressed, which differ in their activity, response to stimuli, and the type of ROS released. Reactive Oxygen Species 157-160 NADPH oxidase 1 Homo sapiens 46-50 22834042-0 2010 Optimization and Characterization of an Inhibitor for NADPH Oxidase 1 (NOX-1) The NADPH oxidase (NOX) family catalyzes the regulated formation of reactive oxygen species (ROS). Reactive Oxygen Species 146-169 NADPH oxidase 1 Homo sapiens 54-69 22834042-0 2010 Optimization and Characterization of an Inhibitor for NADPH Oxidase 1 (NOX-1) The NADPH oxidase (NOX) family catalyzes the regulated formation of reactive oxygen species (ROS). Reactive Oxygen Species 146-169 NADPH oxidase 1 Homo sapiens 71-76 22834042-0 2010 Optimization and Characterization of an Inhibitor for NADPH Oxidase 1 (NOX-1) The NADPH oxidase (NOX) family catalyzes the regulated formation of reactive oxygen species (ROS). Reactive Oxygen Species 171-174 NADPH oxidase 1 Homo sapiens 54-69 22834042-0 2010 Optimization and Characterization of an Inhibitor for NADPH Oxidase 1 (NOX-1) The NADPH oxidase (NOX) family catalyzes the regulated formation of reactive oxygen species (ROS). Reactive Oxygen Species 171-174 NADPH oxidase 1 Homo sapiens 71-76 22834042-1 2010 ROS generated via NOX1 have been reported to play a role in a growing number of diseases, including cancer, atherosclerosis, hypertension, neurological disorders and inflammation. Reactive Oxygen Species 0-3 NADPH oxidase 1 Homo sapiens 18-22 22834042-2 2010 Since ROS are also produced by other cellular enzymes, the ability to selectively inhibit NOX1 can be expected to provide reversible, mechanistic insights into these cellular processes with which it is involved. Reactive Oxygen Species 6-9 NADPH oxidase 1 Homo sapiens 90-94 22834042-7 2010 These results elucidate the relevance of NOX1-dependent ROS generation in mechanisms of cancer invasion, and define compound ML171 as a powerful NOX1 chemical probe and a potential therapeutic agent for treatment of this pathology. Reactive Oxygen Species 56-59 NADPH oxidase 1 Homo sapiens 41-45 21252614-6 2011 Further experiments aimed at elucidating the mechanism by which BLT2 mediates survival revealed that enhanced level of reactive oxygen species (ROS) are generated via a BLT2-dependent up-regulation of NADPH oxidase members NOX1 and NOX4. Reactive Oxygen Species 119-142 NADPH oxidase 1 Homo sapiens 223-227 21723410-0 2011 NOX1 participates in ROS-dependent cell death of colon epithelial Caco2 cells induced by Entamoeba histolytica. Reactive Oxygen Species 21-24 NADPH oxidase 1 Homo sapiens 0-4 21723410-7 2011 siRNA-mediated suppression of NOX1 protein significantly inhibited E. histolytica-induced cell death and ROS response in Caco2 cells. Reactive Oxygen Species 105-108 NADPH oxidase 1 Homo sapiens 30-34 21723410-8 2011 These results suggest that NOX1 participates in the ROS-dependent cell death of colon epithelial cells induced by amebic adhesion during the early phase of intestinal amebiasis. Reactive Oxygen Species 52-55 NADPH oxidase 1 Homo sapiens 27-31 21962117-2 2011 NOX/NADPH oxidases generate reactive oxygen species and NOX1, NOX2 and NOX4 isoforms are expressed in kidney and require association with subunit p22phox (encoded by the CYBA gene). Reactive Oxygen Species 28-51 NADPH oxidase 1 Homo sapiens 56-60 21586323-1 2011 In recent years, reactive oxygen species (ROS) derived from the vascular isoforms of NADPH oxidase, Nox1, Nox2, and Nox4, have been implicated in many cardiovascular pathologies. Reactive Oxygen Species 17-40 NADPH oxidase 1 Homo sapiens 100-104 21586323-1 2011 In recent years, reactive oxygen species (ROS) derived from the vascular isoforms of NADPH oxidase, Nox1, Nox2, and Nox4, have been implicated in many cardiovascular pathologies. Reactive Oxygen Species 42-45 NADPH oxidase 1 Homo sapiens 100-104 21167810-0 2011 XPC silencing in normal human keratinocytes triggers metabolic alterations through NOX-1 activation-mediated reactive oxygen species. Reactive Oxygen Species 109-132 NADPH oxidase 1 Homo sapiens 83-88 21167810-3 2011 We showed that knockdown of XPC (XPC(KD)) in normal human keratinocytes results in metabolism remodeling through NADPH oxidase-1 (NOX-1) activation, which in turn leads to increased ROS levels. Reactive Oxygen Species 182-185 NADPH oxidase 1 Homo sapiens 130-135 21167810-4 2011 While enforcing antioxidant defenses by overexpressing catalase, CuZnSOD, or MnSOD could not block the metabolism remodeling, impaired NOX-1 activation abrogates both alteration in ROS levels and modifications of energy metabolism. Reactive Oxygen Species 181-184 NADPH oxidase 1 Homo sapiens 135-140 21629295-2 2011 The NOX1 (NADPH oxidase 1) and NOX2 oxidases are the major sources of ROS in the artery wall in conditions such as hypertension, hypercholesterolaemia, diabetes and ageing, and so they are important contributors to the oxidative stress, endothelial dysfunction and vascular inflammation that underlies arterial remodelling and atherogenesis. Reactive Oxygen Species 70-73 NADPH oxidase 1 Homo sapiens 4-8 21629295-2 2011 The NOX1 (NADPH oxidase 1) and NOX2 oxidases are the major sources of ROS in the artery wall in conditions such as hypertension, hypercholesterolaemia, diabetes and ageing, and so they are important contributors to the oxidative stress, endothelial dysfunction and vascular inflammation that underlies arterial remodelling and atherogenesis. Reactive Oxygen Species 70-73 NADPH oxidase 1 Homo sapiens 10-25 21252614-7 2011 Additionally, we observed that inhibition of ROS generation by either NOX1/4 siRNAs or treatment with an ROS-scavenging agent results in apoptotic cell death in 253J-BV bladder cancer cells. Reactive Oxygen Species 45-48 NADPH oxidase 1 Homo sapiens 70-74 21857021-8 2011 Given that Nox1 produces reactive oxygen species, we evaluated their participation in this SSH1L activation mechanism. Reactive Oxygen Species 25-48 NADPH oxidase 1 Homo sapiens 11-15 21507984-8 2011 Based on these results, we concluded that Rac1-dependent NOX1 activity is required for RV- or poly(I:C)-induced ROS generation, which in turn disrupts the barrier function of polarized airway epithelia. Reactive Oxygen Species 112-115 NADPH oxidase 1 Homo sapiens 57-61 21381898-4 2011 A substantial amount of ROS is produced through the NADPH oxidase (NOX) system and knockdown of p22phox, a sub-unit of NOX1-4, resulted not only in reduced ROS levels but also in reduced GGT expression in human endometrial carcinoma cells. Reactive Oxygen Species 24-27 NADPH oxidase 1 Homo sapiens 119-123 21381898-4 2011 A substantial amount of ROS is produced through the NADPH oxidase (NOX) system and knockdown of p22phox, a sub-unit of NOX1-4, resulted not only in reduced ROS levels but also in reduced GGT expression in human endometrial carcinoma cells. Reactive Oxygen Species 156-159 NADPH oxidase 1 Homo sapiens 119-123 21252614-6 2011 Further experiments aimed at elucidating the mechanism by which BLT2 mediates survival revealed that enhanced level of reactive oxygen species (ROS) are generated via a BLT2-dependent up-regulation of NADPH oxidase members NOX1 and NOX4. Reactive Oxygen Species 144-147 NADPH oxidase 1 Homo sapiens 223-227 21039341-2 2011 Of the seven family members, four have been identified as important sources of ROS in the vasculature: Nox1, Nox2, Nox4 and Nox5. Reactive Oxygen Species 79-82 NADPH oxidase 1 Homo sapiens 103-107 21397852-0 2011 Escaping Anoikis through ROS: ANGPTL4 controls integrin signaling through Nox1. Reactive Oxygen Species 25-28 NADPH oxidase 1 Homo sapiens 74-78 21397852-3 2011 demonstrate the ability of ANGPTL4 to engage integrin-dependent survival signals by activation of the NADPH oxidase Nox1, thus mimicking anchorage conditions and bypassing anoikis by controlling ROS. Reactive Oxygen Species 195-198 NADPH oxidase 1 Homo sapiens 116-120 21344509-2 2011 The goal of this study was to investigate the role of the ERK pathway in mediating apoptotic signals induced by oncogenic H-Ras, FK228 treatment, and exogenous H(2) O(2) treatment to increase Nox-1 elevation, leading to production of intracellular reactive oxygen species (ROS) for inducing apoptosis in human bladder cancer J82 cells. Reactive Oxygen Species 248-271 NADPH oxidase 1 Homo sapiens 192-197 21344509-2 2011 The goal of this study was to investigate the role of the ERK pathway in mediating apoptotic signals induced by oncogenic H-Ras, FK228 treatment, and exogenous H(2) O(2) treatment to increase Nox-1 elevation, leading to production of intracellular reactive oxygen species (ROS) for inducing apoptosis in human bladder cancer J82 cells. Reactive Oxygen Species 273-276 NADPH oxidase 1 Homo sapiens 192-197 20473523-10 2011 Knockdown of Nox-1 by specific siRNAs reduced FK228-induced ROS production, caspase activation, and cell death. Reactive Oxygen Species 60-63 NADPH oxidase 1 Homo sapiens 13-18 20609497-0 2011 Direct interaction between Tks proteins and the N-terminal proline-rich region (PRR) of NoxA1 mediates Nox1-dependent ROS generation. Reactive Oxygen Species 118-121 NADPH oxidase 1 Homo sapiens 103-107 20609497-9 2011 When the PRR in NoxA1 is disrupted, Tks proteins cannot bind NoxA1 and lose their ability to support Nox1-dependent ROS generation. Reactive Oxygen Species 116-119 NADPH oxidase 1 Homo sapiens 101-105 20942471-3 2010 SAR investigation around the pyrazolopyridine dione core led to the discovery of several double-digit nanomolar inhibitors in cell free assays of reactive oxygen species (ROS) production, showing high potency on Nox4 and Nox1. Reactive Oxygen Species 146-169 NADPH oxidase 1 Homo sapiens 221-225 20981034-6 2011 A major source for cardiovascular, renal and neural ROS is a family of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox), including the prototypic Nox2 homolog-based NADPH oxidase, as well as other Noxes, such as Nox1 and Nox4. Reactive Oxygen Species 52-55 NADPH oxidase 1 Homo sapiens 245-249 20883826-2 2010 Of the several potential sources of ROS in the vasculature, the endothelial NADPH oxidase (Nox) family of proteins, Nox1, Nox2, Nox4 and Nox5, are major contributors of ROS. Reactive Oxygen Species 36-39 NADPH oxidase 1 Homo sapiens 116-120 20883826-2 2010 Of the several potential sources of ROS in the vasculature, the endothelial NADPH oxidase (Nox) family of proteins, Nox1, Nox2, Nox4 and Nox5, are major contributors of ROS. Reactive Oxygen Species 169-172 NADPH oxidase 1 Homo sapiens 116-120 20943948-1 2010 The NADPH oxidase family, consisting of Nox1-5 and Duox1-2, catalyzes the regulated formation of reactive oxygen species (ROS). Reactive Oxygen Species 97-120 NADPH oxidase 1 Homo sapiens 40-44 20943948-1 2010 The NADPH oxidase family, consisting of Nox1-5 and Duox1-2, catalyzes the regulated formation of reactive oxygen species (ROS). Reactive Oxygen Species 122-125 NADPH oxidase 1 Homo sapiens 40-44 20943948-5 2010 Nox1-dependent ROS generation is necessary for the maintenance of functional invadopodia in human colon cancer cells. Reactive Oxygen Species 15-18 NADPH oxidase 1 Homo sapiens 0-4 20943948-8 2010 Interestingly, the abolishment of Src-mediated phosphorylation of Tyr110 on NoxA1 and of Tyr508 on Tks4 blocks their binding and decreases Nox1-dependent ROS generation. Reactive Oxygen Species 154-157 NADPH oxidase 1 Homo sapiens 139-143 20952677-6 2010 Additionally, we found that the generation of Nox1-derived reactive oxygen species occurs downstream of BLT2, thus mediating the synthesis of Th2 cytokines. Reactive Oxygen Species 59-82 NADPH oxidase 1 Homo sapiens 46-50 20942471-3 2010 SAR investigation around the pyrazolopyridine dione core led to the discovery of several double-digit nanomolar inhibitors in cell free assays of reactive oxygen species (ROS) production, showing high potency on Nox4 and Nox1. Reactive Oxygen Species 171-174 NADPH oxidase 1 Homo sapiens 221-225 20715845-2 2010 ROS generation by the Nox1 member of the Nox family is necessary for the formation of extracellular matrix (ECM)-degrading, actin-rich cellular structures known as invadopodia. Reactive Oxygen Species 0-3 NADPH oxidase 1 Homo sapiens 22-26 20715845-8 2010 These results elucidate the relevance of Nox1-dependent ROS generation in mechanisms of cancer invasion and define ML171 as a useful Nox1 chemical probe and potential therapeutic agent for inhibition of cancer cell invasion. Reactive Oxygen Species 56-59 NADPH oxidase 1 Homo sapiens 41-45 20700043-6 2010 Thus, the pro-apoptotic abilities of Mek1/2 and Nox-1 should be considered as potential targets in designing therapeutic protocols using FK228 to assure ROS-mediated cell death for treating cancer cells acquiring Ras activation. Reactive Oxygen Species 153-156 NADPH oxidase 1 Homo sapiens 48-53 20570727-4 2010 IL-13 stimulates intracellular ROS synthesis within 5min via IL-13Ralpha1-JAK1-STAT6- and IL-13Ralpha2-MEK1/2-ERK1/2-dependent activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-1 (NOX-1). Reactive Oxygen Species 31-34 NADPH oxidase 1 Homo sapiens 141-202 20700043-0 2010 FK228 and oncogenic H-Ras synergistically induce Mek1/2 and Nox-1 to generate reactive oxygen species for differential cell death. Reactive Oxygen Species 78-101 NADPH oxidase 1 Homo sapiens 60-65 20570727-4 2010 IL-13 stimulates intracellular ROS synthesis within 5min via IL-13Ralpha1-JAK1-STAT6- and IL-13Ralpha2-MEK1/2-ERK1/2-dependent activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-1 (NOX-1). Reactive Oxygen Species 31-34 NADPH oxidase 1 Homo sapiens 204-209 20570727-6 2010 IL-13 also stimulates the stable, long-term gene expression of two other NADPH oxidases, NOX-4 and DUOX-2, which along with constitutive NOX-1, might facilitate elevated, continuous production of ROS in IL-13-activated IEC. Reactive Oxygen Species 196-199 NADPH oxidase 1 Homo sapiens 137-142 21433358-0 2010 Probe Report for NOX1 Inhibitors NADPH oxidase 1 (NOX1) is highly expressed in colon epithelial cells, where it generates reactive oxygen species (ROS) to interact with normal and pathogenic bacteria. Reactive Oxygen Species 122-145 NADPH oxidase 1 Homo sapiens 17-21 20600831-5 2010 Moreover, our results demonstrated that BLT2 mediates invasiveness through a signaling pathway dependent on NAD(P)H oxidase (Nox) 1- and Nox4-induced generation of reactive oxygen species (ROS) and subsequent NF-kappaB stimulation. Reactive Oxygen Species 164-187 NADPH oxidase 1 Homo sapiens 108-131 20600831-5 2010 Moreover, our results demonstrated that BLT2 mediates invasiveness through a signaling pathway dependent on NAD(P)H oxidase (Nox) 1- and Nox4-induced generation of reactive oxygen species (ROS) and subsequent NF-kappaB stimulation. Reactive Oxygen Species 189-192 NADPH oxidase 1 Homo sapiens 108-131 21433358-0 2010 Probe Report for NOX1 Inhibitors NADPH oxidase 1 (NOX1) is highly expressed in colon epithelial cells, where it generates reactive oxygen species (ROS) to interact with normal and pathogenic bacteria. Reactive Oxygen Species 122-145 NADPH oxidase 1 Homo sapiens 33-48 21433358-0 2010 Probe Report for NOX1 Inhibitors NADPH oxidase 1 (NOX1) is highly expressed in colon epithelial cells, where it generates reactive oxygen species (ROS) to interact with normal and pathogenic bacteria. Reactive Oxygen Species 122-145 NADPH oxidase 1 Homo sapiens 50-54 21433358-0 2010 Probe Report for NOX1 Inhibitors NADPH oxidase 1 (NOX1) is highly expressed in colon epithelial cells, where it generates reactive oxygen species (ROS) to interact with normal and pathogenic bacteria. Reactive Oxygen Species 147-150 NADPH oxidase 1 Homo sapiens 17-21 21433358-0 2010 Probe Report for NOX1 Inhibitors NADPH oxidase 1 (NOX1) is highly expressed in colon epithelial cells, where it generates reactive oxygen species (ROS) to interact with normal and pathogenic bacteria. Reactive Oxygen Species 147-150 NADPH oxidase 1 Homo sapiens 33-48 21433358-0 2010 Probe Report for NOX1 Inhibitors NADPH oxidase 1 (NOX1) is highly expressed in colon epithelial cells, where it generates reactive oxygen species (ROS) to interact with normal and pathogenic bacteria. Reactive Oxygen Species 147-150 NADPH oxidase 1 Homo sapiens 50-54 20177149-5 2010 More precisely, gene knockdown by shRNA for either Nox-1 or Nox-4 isozyme of gp91phox subunit of NADPH oxidase abolished both the early time ROS production and migration. Reactive Oxygen Species 141-144 NADPH oxidase 1 Homo sapiens 51-56 20578128-9 2010 HCV-induced ROS and nuclear nitrotyrosine could be decreased with small interfering RNAs to Nox1 and Nox4. Reactive Oxygen Species 12-15 NADPH oxidase 1 Homo sapiens 92-96 20110267-2 2010 NOX1 is expressed mainly in colon epithelial cells and could be involved in mucosal innate immunity by producing reactive oxygen species (ROS). Reactive Oxygen Species 113-136 NADPH oxidase 1 Homo sapiens 0-4 20110267-2 2010 NOX1 is expressed mainly in colon epithelial cells and could be involved in mucosal innate immunity by producing reactive oxygen species (ROS). Reactive Oxygen Species 138-141 NADPH oxidase 1 Homo sapiens 0-4 20110267-7 2010 Indeed, S172A and S282A single mutants of NOXA1 significantly up-regulated constitutive NOX1-derived ROS production, and S172A/S282A double mutant further increased it, as compared to wild-type NOXA1. Reactive Oxygen Species 101-104 NADPH oxidase 1 Homo sapiens 88-92 20122895-6 2010 The third model was based on cell death by serum withdrawal that promotes the production of ROS in human 293T cells by stimulating both the mitochondria and Nox1. Reactive Oxygen Species 92-95 NADPH oxidase 1 Homo sapiens 157-161 20122895-7 2010 By superior molecular biological methods the authors showed that mitochondria were responsible for the fast onset of ROS formation followed by a slower but long-lasting oxidative stress condition based on the activation of an NADPH oxidase (Nox1) in response to the fast mitochondrial ROS formation. Reactive Oxygen Species 285-288 NADPH oxidase 1 Homo sapiens 241-245 19737091-2 2010 The aim of this study was to test the hypothesis that endocytosis is necessary for generation of reactive oxygen species (ROS) by Nox1 and for redox-dependent signaling in smooth muscle cells (SMCs). Reactive Oxygen Species 97-120 NADPH oxidase 1 Homo sapiens 130-134 19748928-5 2010 Expression of Nox1, a member of the NADPH oxidase family, is also highly upregulated in a BLT2-dependent manner in these breast cancer cells, suggesting that "Nox1-derived ROS" lie downstream of BLT2. Reactive Oxygen Species 172-175 NADPH oxidase 1 Homo sapiens 14-18 19748928-5 2010 Expression of Nox1, a member of the NADPH oxidase family, is also highly upregulated in a BLT2-dependent manner in these breast cancer cells, suggesting that "Nox1-derived ROS" lie downstream of BLT2. Reactive Oxygen Species 172-175 NADPH oxidase 1 Homo sapiens 159-163 19748928-6 2010 Consistent with the proposed role of "Nox1-ROS" in pro-survival signaling, knockdown of Nox1 with siNox1 or treatment with a ROS scavenging agent caused dramatic apoptotic death in these breast cancer cells. Reactive Oxygen Species 43-46 NADPH oxidase 1 Homo sapiens 38-42 19748928-6 2010 Consistent with the proposed role of "Nox1-ROS" in pro-survival signaling, knockdown of Nox1 with siNox1 or treatment with a ROS scavenging agent caused dramatic apoptotic death in these breast cancer cells. Reactive Oxygen Species 43-46 NADPH oxidase 1 Homo sapiens 88-92 20090768-4 2010 Moreover, we found that the NADPH oxidase family protein Nox1 lies downstream of BLT2 and mediates UVB-induced ROS production and apoptosis. Reactive Oxygen Species 111-114 NADPH oxidase 1 Homo sapiens 57-61 20090768-7 2010 Taken together, our results demonstrate that a "BLT2-Nox1"-linked pathway has a crucial role in UVB-induced ROS generation and mediates apoptosis in human keratinocytes. Reactive Oxygen Species 108-111 NADPH oxidase 1 Homo sapiens 53-57 19910640-2 2010 Four members of the NADPH oxidase (Nox) enzyme family are important sources of reactive oxygen species in the vasculature: Nox1, Nox2, Nox4, and Nox5. Reactive Oxygen Species 79-102 NADPH oxidase 1 Homo sapiens 123-127 20237264-7 2010 Furthermore, suppression of NOX1 and NOX4 expression by small interfering RNA transfection markedly abolished the cytotoxicity and ROS generation by cisplatin. Reactive Oxygen Species 131-134 NADPH oxidase 1 Homo sapiens 28-32 19737091-2 2010 The aim of this study was to test the hypothesis that endocytosis is necessary for generation of reactive oxygen species (ROS) by Nox1 and for redox-dependent signaling in smooth muscle cells (SMCs). Reactive Oxygen Species 122-125 NADPH oxidase 1 Homo sapiens 130-134 19737091-3 2010 Within minutes of treatment with tumor necrosis factor (TNF)-alpha or thrombin, SMCs increased cellular levels of ROS that was inhibited by shRNA to Nox1. Reactive Oxygen Species 114-117 NADPH oxidase 1 Homo sapiens 149-153 20368025-6 2010 Nox1 siRNA inhibited ROS activity (0.19 +/- 0.06), reduced MUC5AC protein (0.31 +/- 0.05) and mRNA level (0.32 +/- 0.06), compared with single NE-stimulated group, P < 0.01. Reactive Oxygen Species 21-24 NADPH oxidase 1 Homo sapiens 0-4 20368025-7 2010 c-src siRNA and PP2 also showed the same effects, both of them decreased the NE-induced high activity of ROS, was 0.29 +/- 0.05, and 0.41 +/- 0.11, respectively, the MUC5AC protein in the c-src siRNA group and PP2 group were 0.38 +/- 0.09 and 0.48 +/- 0.08, MUC5AC mRNA level were 0.41 +/- 0.04 and 0.46 +/- 0.07, the Nox1 protein were 0.39 +/- 0.08 and 0.44 +/- 0.05, all P < 0.05, compared with single NE-treated group. Reactive Oxygen Species 105-108 NADPH oxidase 1 Homo sapiens 318-322 19733235-5 2009 In HG, the mRNA levels of Nox1 and Nox4 and the protein level of Nox4 were increased; knocking down Nox1 or Nox4 attenuated the ROS production and restored the inhibition of SMC migration by NO. Reactive Oxygen Species 128-131 NADPH oxidase 1 Homo sapiens 100-104 19628035-2 2009 ROS produced by Nox proteins Nox1-5 and Duox1/2 are now recognized to play essential roles in the physiology of the brain, the immune system, the vasculature, and the digestive tract as well as in hormone synthesis. Reactive Oxygen Species 0-3 NADPH oxidase 1 Homo sapiens 29-33 19917703-2 2009 This study reveals the control mechanism of the gene for NADPH oxidase 1 (Nox1), which produces ROS in the formation of foam cells by stimulating TLR4. Reactive Oxygen Species 96-99 NADPH oxidase 1 Homo sapiens 57-72 19917703-2 2009 This study reveals the control mechanism of the gene for NADPH oxidase 1 (Nox1), which produces ROS in the formation of foam cells by stimulating TLR4. Reactive Oxygen Species 96-99 NADPH oxidase 1 Homo sapiens 74-78 19917703-6 2009 Small interfering RNA mediated inhibition of Nox1 expression decreased LPS-induced ROS production and foam cell formation. Reactive Oxygen Species 83-86 NADPH oxidase 1 Homo sapiens 45-49 19755710-4 2009 Endogenous Tks4 is required for Rac guanosine triphosphatase- and Nox1-dependent ROS production by DLD1 colon cancer cells. Reactive Oxygen Species 81-84 NADPH oxidase 1 Homo sapiens 66-70 19543237-4 2009 Rac1 GTPase and NADPH oxidase 1 (Nox1) are activated by IL-17 to produce ROS, which in turn stimulates hMSC proliferation. Reactive Oxygen Species 73-76 NADPH oxidase 1 Homo sapiens 16-31 19543237-4 2009 Rac1 GTPase and NADPH oxidase 1 (Nox1) are activated by IL-17 to produce ROS, which in turn stimulates hMSC proliferation. Reactive Oxygen Species 73-76 NADPH oxidase 1 Homo sapiens 33-37 19328228-8 2009 Using an siRNA approach, we clearly identified two NADPH oxidases, Nox1 and Nox4, as major targets of resveratrol and primary sources of ROS that act upstream of the observed S-phase accumulation. Reactive Oxygen Species 137-140 NADPH oxidase 1 Homo sapiens 67-71 19671250-6 2009 CONCLUSIONS: These results indicate that NOX1 and NOX4 may play an important role in reactive oxygen species production, contributing to the oxidative stress in allergic rhinitis and nasal polyp tissues. Reactive Oxygen Species 85-108 NADPH oxidase 1 Homo sapiens 41-45 19293182-6 2009 These findings indicate an essential role for ALKBH8 in urothelial carcinoma cell survival mediated by NOX-1-dependent ROS signals, further suggesting new therapeutic strategies in human bladder cancer by inducing JNK/p38/gammaH2AX-mediated cell death by silencing of ALKBH8. Reactive Oxygen Species 119-122 NADPH oxidase 1 Homo sapiens 103-108 19057021-2 2009 Insulin also stimulates reactive oxygen species (ROS) production, and the NADPH oxidases Nox1 and Nox4 are important sources of ROS. Reactive Oxygen Species 128-131 NADPH oxidase 1 Homo sapiens 89-93 19057021-4 2009 METHODS AND RESULTS: The expression of Nox1 and Nox4 was increased during insulin-induced differentiation, and insulin increased ROS production. Reactive Oxygen Species 129-132 NADPH oxidase 1 Homo sapiens 39-43 19714290-11 2009 CONCLUSIONS: IL-10 may be a possible down-regulator of the Nox1-based oxidase in the colon, suggesting a potential role of reactive oxygen species (ROS) derived from Nox1-based oxidase in inflammation of the colon. Reactive Oxygen Species 123-146 NADPH oxidase 1 Homo sapiens 166-170 19714290-11 2009 CONCLUSIONS: IL-10 may be a possible down-regulator of the Nox1-based oxidase in the colon, suggesting a potential role of reactive oxygen species (ROS) derived from Nox1-based oxidase in inflammation of the colon. Reactive Oxygen Species 148-151 NADPH oxidase 1 Homo sapiens 59-63 19714290-11 2009 CONCLUSIONS: IL-10 may be a possible down-regulator of the Nox1-based oxidase in the colon, suggesting a potential role of reactive oxygen species (ROS) derived from Nox1-based oxidase in inflammation of the colon. Reactive Oxygen Species 148-151 NADPH oxidase 1 Homo sapiens 166-170 18957266-2 2008 Here, we show that immediately after ligand-dependent activation, interleukin (IL)-4 receptor generated reactive oxygen species (ROS) via phosphatidylinositol 3-kinase-dependent activation of NAD(P)H oxidase (NOX)1 and NOX5L. Reactive Oxygen Species 104-127 NADPH oxidase 1 Homo sapiens 192-214 20046221-0 2009 Anthrax edema toxin inhibits Nox1-mediated formation of reactive oxygen species by colon epithelial cells. Reactive Oxygen Species 56-79 NADPH oxidase 1 Homo sapiens 29-33 20046221-3 2009 NADPH oxidase enzymes (Nox1-Nox5, Duox1 and 2) generate reactive oxygen species (ROS) as components of the host innate immune response to bacteria, including Nox1 in gastrointestinal epithelial tissues. Reactive Oxygen Species 56-79 NADPH oxidase 1 Homo sapiens 23-27 20046221-3 2009 NADPH oxidase enzymes (Nox1-Nox5, Duox1 and 2) generate reactive oxygen species (ROS) as components of the host innate immune response to bacteria, including Nox1 in gastrointestinal epithelial tissues. Reactive Oxygen Species 56-79 NADPH oxidase 1 Homo sapiens 158-162 20046221-3 2009 NADPH oxidase enzymes (Nox1-Nox5, Duox1 and 2) generate reactive oxygen species (ROS) as components of the host innate immune response to bacteria, including Nox1 in gastrointestinal epithelial tissues. Reactive Oxygen Species 81-84 NADPH oxidase 1 Homo sapiens 23-27 20046221-3 2009 NADPH oxidase enzymes (Nox1-Nox5, Duox1 and 2) generate reactive oxygen species (ROS) as components of the host innate immune response to bacteria, including Nox1 in gastrointestinal epithelial tissues. Reactive Oxygen Species 81-84 NADPH oxidase 1 Homo sapiens 158-162 20046221-4 2009 We show that ETx effectively inhibits ROS formation by Nox1 in HT-29 colon epithelial cells. Reactive Oxygen Species 38-41 NADPH oxidase 1 Homo sapiens 55-59 20046221-6 2009 Inhibition of Nox1-mediated ROS formation in the gut epithelium may be a mechanism used by B. anthracis to circumvent the innate immune response. Reactive Oxygen Species 28-31 NADPH oxidase 1 Homo sapiens 14-18 18620548-2 2008 In the present study we show that one of the proteins selectively oxidized in response to Nox1-generated ROS was ERp72 (endoplasmic reticulum protein 72 kDa) with TRX (thioredoxin) homology domains. Reactive Oxygen Species 105-108 NADPH oxidase 1 Homo sapiens 90-94 18957266-2 2008 Here, we show that immediately after ligand-dependent activation, interleukin (IL)-4 receptor generated reactive oxygen species (ROS) via phosphatidylinositol 3-kinase-dependent activation of NAD(P)H oxidase (NOX)1 and NOX5L. Reactive Oxygen Species 129-132 NADPH oxidase 1 Homo sapiens 192-214 18406051-7 2008 Major source of ROS in ECs is a NADPH oxidase which consists of Nox1, Nox2, Nox4, Nox5, p22phox, p47phox and the small G-protein Rac1. Reactive Oxygen Species 16-19 NADPH oxidase 1 Homo sapiens 64-68 18454176-1 2008 Ras oncogene upregulates the expression of nicotinamide adenine dinucleotide phosphate oxidase (Nox) 1 via the Raf/MEK/ERK pathway, leading to the elevated production of reactive oxygen species that is essential for maintenance of Ras-transformation phenotypes. Reactive Oxygen Species 170-193 NADPH oxidase 1 Homo sapiens 43-102 18463161-0 2008 The involvement of the tyrosine kinase c-Src in the regulation of reactive oxygen species generation mediated by NADPH oxidase-1. Reactive Oxygen Species 66-89 NADPH oxidase 1 Homo sapiens 113-128 18463161-5 2008 In this study, we investigate the role of the tyrosine kinase c-Src in the regulation of ROS formation by Nox1. Reactive Oxygen Species 89-92 NADPH oxidase 1 Homo sapiens 106-110 18463161-6 2008 We show that c-Src induces Nox1-mediated ROS generation in the HT29 human colon carcinoma cell line through a Rac-dependent mechanism. Reactive Oxygen Species 41-44 NADPH oxidase 1 Homo sapiens 27-31 18463161-9 2008 Consistent with this, Vav2 siRNA that specifically reduces endogenous Vav2 protein is able to dramatically decrease Nox1-dependent ROS generation and abolish c-Src-induced Nox1 activity. Reactive Oxygen Species 131-134 NADPH oxidase 1 Homo sapiens 116-120 18035043-4 2008 Nox1-mRNA was upregulated by gamma-ray irradiation in NS-SV-AC, and the ROS level in NS-SV-AC was increased to approximately threefold of the control level after 10Gy irradiation. Reactive Oxygen Species 72-75 NADPH oxidase 1 Homo sapiens 0-4 18082638-5 2008 Taken together, our results suggest that a BLT2-Nox1-linked cascade is responsible for the elevated ROS generation in Ras-transformed cells. Reactive Oxygen Species 100-103 NADPH oxidase 1 Homo sapiens 48-52 18035043-5 2008 The increase of ROS level in NS-SV-AC was suppressed by Nox1-siRNA-transfection. Reactive Oxygen Species 16-19 NADPH oxidase 1 Homo sapiens 56-60 18035043-8 2008 In conclusion, these results indicate that Nox1 plays a crucial role in irradiation-induced ROS generation and ROS-associated impairment of salivary gland cells and that Nox1 gene may be targeted for preservation of the salivary gland function from radiation-induced impairment. Reactive Oxygen Species 92-95 NADPH oxidase 1 Homo sapiens 43-47 18035043-8 2008 In conclusion, these results indicate that Nox1 plays a crucial role in irradiation-induced ROS generation and ROS-associated impairment of salivary gland cells and that Nox1 gene may be targeted for preservation of the salivary gland function from radiation-induced impairment. Reactive Oxygen Species 111-114 NADPH oxidase 1 Homo sapiens 43-47 17390063-0 2007 Ionizing radiation-induced micronucleus formation is mediated by reactive oxygen species that are produced in a manner dependent on mitochondria, Nox1, and JNK. Reactive Oxygen Species 65-88 NADPH oxidase 1 Homo sapiens 146-150 18227481-3 2008 A major source for vascular and renal ROS is a family of nonphagocytic NAD(P)H oxidases, including the prototypic Nox2 homolog-based NAD(P)H oxidase, as well as other NAD(P)H oxidases, such as Nox1 and Nox4. Reactive Oxygen Species 38-41 NADPH oxidase 1 Homo sapiens 193-197 18287880-6 2008 In cultured venous SMC under unstimulated conditions, inhibition of nox1 or nox2 mRNA decreased ROS production, whereas p47 silencing increased it. Reactive Oxygen Species 96-99 NADPH oxidase 1 Homo sapiens 68-72 18287880-9 2008 Only nox2 is implicated in response to AngII whilst nox1 is involved in unstimulated ROS production. Reactive Oxygen Species 85-88 NADPH oxidase 1 Homo sapiens 52-56 17611574-0 2008 Nox1-based NADPH oxidase is the major source of UVA-induced reactive oxygen species in human keratinocytes. Reactive Oxygen Species 60-83 NADPH oxidase 1 Homo sapiens 0-4 17611574-5 2008 Depleting the Nox1 isoform of the catalytic subunit of NADPH oxidase using small interfering RNA (siRNA) blocked the UVA-induced ROS increase, indicating that ROS produced by mitochondria or other sources are downstream from Nox1. Reactive Oxygen Species 129-132 NADPH oxidase 1 Homo sapiens 14-18 17611574-5 2008 Depleting the Nox1 isoform of the catalytic subunit of NADPH oxidase using small interfering RNA (siRNA) blocked the UVA-induced ROS increase, indicating that ROS produced by mitochondria or other sources are downstream from Nox1. Reactive Oxygen Species 129-132 NADPH oxidase 1 Homo sapiens 225-229 17611574-5 2008 Depleting the Nox1 isoform of the catalytic subunit of NADPH oxidase using small interfering RNA (siRNA) blocked the UVA-induced ROS increase, indicating that ROS produced by mitochondria or other sources are downstream from Nox1. Reactive Oxygen Species 159-162 NADPH oxidase 1 Homo sapiens 14-18 17611574-5 2008 Depleting the Nox1 isoform of the catalytic subunit of NADPH oxidase using small interfering RNA (siRNA) blocked the UVA-induced ROS increase, indicating that ROS produced by mitochondria or other sources are downstream from Nox1. Reactive Oxygen Species 159-162 NADPH oxidase 1 Homo sapiens 225-229 17611574-9 2008 These results indicate that UVA activates Nox1-based NADPH oxidase to produce ROS that stimulate PGE2 synthesis, and that Nox1 may be an appropriate target for agents designed to block UVA-induced skin injury. Reactive Oxygen Species 78-81 NADPH oxidase 1 Homo sapiens 42-46 17913709-8 2007 Our data establish that PKA-phosphorylated NoxA1 is a new binding partner of 14-3-3 protein(s) and that this forms the basis of a novel mechanism regulating the formation of ROS by Nox1 and, potentially, other NoxA1-regulated Nox family members. Reactive Oxygen Species 174-177 NADPH oxidase 1 Homo sapiens 181-185 17673675-8 2007 ClC-3, an anion transporter that is primarily found in intracellular vesicles, also colocalized with Nox1 in early endosomes and was necessary for tumor necrosis factor-alpha and interleukin-1beta generation of ROS. Reactive Oxygen Species 211-214 NADPH oxidase 1 Homo sapiens 101-105 17588511-3 2007 (2007) reported on a novel TNF receptor 1 necrotic signaling complex inducing TRADD- and RIP1-dependent recruitment and activation of the ROS-generating Nox1 NADPH oxidase complex. Reactive Oxygen Species 138-141 NADPH oxidase 1 Homo sapiens 153-157 17963706-3 2008 Transfectants of mismatch repair (MMR)-proficient HeLa cells or MMR-defective Msh2(-/-) mouse embryo fibroblasts overexpressing the hNOX1 complex displayed increased intracellular ROS levels. Reactive Oxygen Species 180-183 NADPH oxidase 1 Homo sapiens 132-137 18206804-3 2008 Reactive oxygen species formation by the nicotinamide adenine dinucleotide phosphate oxidases Nox1 and Nox2 in arteries is a consequence of an activation of the enzymes by different stimuli such as growth factors, cytokines, and cardiovascular risk factors (cigarette smoke, high blood pressure, oxidized lipids). Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 94-98 18206804-5 2008 The negative vascular effects of ROS, such as endothelial dysfunction, vascular hypertrophy, aneurysm formation, and inflammatory activation, appear to be the consequence of an activation of Nox1 and Nox2. Reactive Oxygen Species 33-36 NADPH oxidase 1 Homo sapiens 191-195 18037128-7 2007 Thus, the Nox1-base oxidase may be a potential marker of neoplastic transformation and play an important role in oxygen radical- and inflammation-dependent carcinogenesis in the human stomach. Reactive Oxygen Species 113-127 NADPH oxidase 1 Homo sapiens 10-14 18055552-3 2007 Increased ROS and tumor growth in the Nox1-overexpressing DU145 cells were reversed in the presence of the Nox1RNAi. Reactive Oxygen Species 10-13 NADPH oxidase 1 Homo sapiens 38-42 17913709-1 2007 Nox activator 1 (NoxA1) is a homologue of p67(phox) that acts in conjunction with Nox organizer 1 (NoxO1) to regulate reactive oxygen species (ROS) production by the NADPH oxidase Nox1. Reactive Oxygen Species 118-141 NADPH oxidase 1 Homo sapiens 180-184 17913709-1 2007 Nox activator 1 (NoxA1) is a homologue of p67(phox) that acts in conjunction with Nox organizer 1 (NoxO1) to regulate reactive oxygen species (ROS) production by the NADPH oxidase Nox1. Reactive Oxygen Species 143-146 NADPH oxidase 1 Homo sapiens 180-184 17390063-6 2007 The ability of IR to induce the accumulation of ROS and micronucleus formation was also reduced either when the cells were irradiated in the presence of rotenone, a mitochondrial respiratory chain inhibitor, or when the cellular Nox1 levels were reduced by RNA interference. Reactive Oxygen Species 48-51 NADPH oxidase 1 Homo sapiens 229-233 17390063-7 2007 These results suggest that IR stimulates both the mitochondria and Nox1 to produce ROS, and that these ROS are involved in the IR-induced formation of micronuclei. Reactive Oxygen Species 83-86 NADPH oxidase 1 Homo sapiens 67-71 17390063-7 2007 These results suggest that IR stimulates both the mitochondria and Nox1 to produce ROS, and that these ROS are involved in the IR-induced formation of micronuclei. Reactive Oxygen Species 103-106 NADPH oxidase 1 Homo sapiens 67-71 17145559-4 2006 UVA-induced ROS and PGE(2) production were inhibited in these cells by depleting the Nox1 subunit of NADPH oxidase using siRNA or using a mitochondrial radical quencher, MitoQ. Reactive Oxygen Species 12-15 NADPH oxidase 1 Homo sapiens 85-89 16926363-4 2006 NADPH (nicotinamide adenine dinucleotide phosphate) oxidase is one of the major sources of ROS in vasculature; it consists of a catalytic subunit (Nox1, Nox2, Nox3, Nox4, or Nox5), p22phox, p47phox, p67phox, and the small guanosine triphosphatase Rac1. Reactive Oxygen Species 91-94 NADPH oxidase 1 Homo sapiens 147-151 17015444-0 2006 Link between mitochondria and NADPH oxidase 1 isozyme for the sustained production of reactive oxygen species and cell death. Reactive Oxygen Species 86-109 NADPH oxidase 1 Homo sapiens 30-45 17015444-2 2006 This study has shown that serum withdrawal promotes the production of ROS in human 293T cells by stimulating both the mitochondria and Nox1. Reactive Oxygen Species 70-73 NADPH oxidase 1 Homo sapiens 135-139 17015444-3 2006 An analysis of their relationship revealed that the mitochondria respond to serum withdrawal within a few minutes, and the ROS produced by the mitochondria trigger Nox1 action by stimulating phosphoinositide 3-kinase (PI3K) and Rac1. Reactive Oxygen Species 123-126 NADPH oxidase 1 Homo sapiens 164-168 17015444-5 2006 Functional analysis suggested that, although the mitochondria contribute to the early (0-4 h) accumulation of ROS, the maintenance of the induced ROS levels to the later (4-8 h) phase required the action of the PI3K/Rac1/Nox1 pathway. Reactive Oxygen Species 146-149 NADPH oxidase 1 Homo sapiens 221-225 17015444-7 2006 This suggests that mitochondrial ROS are essential but not enough to promote cell death, which requires the sustained accumulation of ROS by the subsequent action of Nox1. Reactive Oxygen Species 33-36 NADPH oxidase 1 Homo sapiens 166-170 17015444-7 2006 This suggests that mitochondrial ROS are essential but not enough to promote cell death, which requires the sustained accumulation of ROS by the subsequent action of Nox1. Reactive Oxygen Species 134-137 NADPH oxidase 1 Homo sapiens 166-170 17015444-8 2006 Overall, this study shows a signaling link between the mitochondria and Nox1, which is crucial for the sustained accumulation of ROS and cell death in serum withdrawal-induced signaling. Reactive Oxygen Species 129-132 NADPH oxidase 1 Homo sapiens 72-76 16987010-2 2006 This enzyme is one representative of the Nox family of oxidases (Nox1-Nox5, Duox1, and Duox2) that exhibit diverse expression patterns and appear to serve a variety of functions related to ROS generation. Reactive Oxygen Species 189-192 NADPH oxidase 1 Homo sapiens 65-69 16987012-6 2006 Nox1-derived reactive oxygen species (ROS) have been implicated in the pathogenesis of inflammation-associated tumor development. Reactive Oxygen Species 13-36 NADPH oxidase 1 Homo sapiens 0-4 16987012-6 2006 Nox1-derived reactive oxygen species (ROS) have been implicated in the pathogenesis of inflammation-associated tumor development. Reactive Oxygen Species 38-41 NADPH oxidase 1 Homo sapiens 0-4 16987012-10 2006 Although Nox1 expression may not be directly linked to mitogenic activity, Nox1-derived ROS may exert a cancer-promoting effect by increasing resistance to programmed cell death of tumor cells. Reactive Oxygen Species 88-91 NADPH oxidase 1 Homo sapiens 75-79 16616784-6 2006 Studies have shown that Nox1, Nox2 (also known as gp91phox) and Nox4 are all expressed in cerebral arteries, suggesting that multiple isoforms of NADPH-oxidase may be important for ROS production by cerebral arteries. Reactive Oxygen Species 181-184 NADPH oxidase 1 Homo sapiens 24-28 16086438-2 2005 NOX1, a ROS-producing NADPH oxidase, is highly expressed in the colon but its function in colonic physiology or pathology is still poorly understood. Reactive Oxygen Species 8-11 NADPH oxidase 1 Homo sapiens 0-4 16781692-5 2006 The major source of ROS in EC is a NADPH oxidase which consists of Nox1, Nox2 (gp91phox), Nox4, p22phox, p47phox, p67phox and the small G protein Rac1. Reactive Oxygen Species 20-23 NADPH oxidase 1 Homo sapiens 67-71 16636067-3 2006 When Nox1 is co-expressed along with its regulatory subunits NOXO1 and NOXA1, significant ROS generation is seen. Reactive Oxygen Species 90-93 NADPH oxidase 1 Homo sapiens 5-9 16636067-5 2006 Decreased Rac1 expression using small interfering RNA reduced Nox1-dependent ROS. Reactive Oxygen Species 77-80 NADPH oxidase 1 Homo sapiens 62-66 16636067-12 2006 A model is presented comparing activation by regulatory subunits of Nox1 versus gp91(phox) (Nox2) in which Rac1 activation provides a major trigger that acutely activates Nox1-dependent ROS generation. Reactive Oxygen Species 186-189 NADPH oxidase 1 Homo sapiens 68-72 16636067-12 2006 A model is presented comparing activation by regulatory subunits of Nox1 versus gp91(phox) (Nox2) in which Rac1 activation provides a major trigger that acutely activates Nox1-dependent ROS generation. Reactive Oxygen Species 186-189 NADPH oxidase 1 Homo sapiens 171-175 16162660-1 2006 NADPH oxidase 1 (Nox1), a homolog of gp91(phox), is dominantly expressed in large intestinal epithelium, and reactive oxygen species derived from Nox1 are suggested to serve a role in host defense. Reactive Oxygen Species 109-132 NADPH oxidase 1 Homo sapiens 0-15 16162660-1 2006 NADPH oxidase 1 (Nox1), a homolog of gp91(phox), is dominantly expressed in large intestinal epithelium, and reactive oxygen species derived from Nox1 are suggested to serve a role in host defense. Reactive Oxygen Species 109-132 NADPH oxidase 1 Homo sapiens 17-21 16162660-1 2006 NADPH oxidase 1 (Nox1), a homolog of gp91(phox), is dominantly expressed in large intestinal epithelium, and reactive oxygen species derived from Nox1 are suggested to serve a role in host defense. Reactive Oxygen Species 109-132 NADPH oxidase 1 Homo sapiens 146-150 16294028-4 2005 Besides mitochondria, NADPH-oxidase 1 (Nox1) also generates a significant amount of ROS in the cell. Reactive Oxygen Species 84-87 NADPH oxidase 1 Homo sapiens 22-37 16294028-4 2005 Besides mitochondria, NADPH-oxidase 1 (Nox1) also generates a significant amount of ROS in the cell. Reactive Oxygen Species 84-87 NADPH oxidase 1 Homo sapiens 39-43 16329988-2 2006 We have previously reported that betaPix, a guanine nucleotide exchange factor for Rac, interacts with NADPH oxidase 1 (Nox1) leading to EGF-induced ROS generation. Reactive Oxygen Species 149-152 NADPH oxidase 1 Homo sapiens 103-118 16329988-2 2006 We have previously reported that betaPix, a guanine nucleotide exchange factor for Rac, interacts with NADPH oxidase 1 (Nox1) leading to EGF-induced ROS generation. Reactive Oxygen Species 149-152 NADPH oxidase 1 Homo sapiens 120-124 16329988-7 2006 These results suggest that the formation of the complex consisting of Nox1, betaPix, and NoxO1 is likely to be a critical step in EGF-induced ROS generation. Reactive Oxygen Species 142-145 NADPH oxidase 1 Homo sapiens 70-74 16083877-0 2005 Reactive oxygen species-linked regulation of the multidrug resistance transporter P-glycoprotein in Nox-1 overexpressing prostate tumor spheroids. Reactive Oxygen Species 0-23 NADPH oxidase 1 Homo sapiens 100-105 15110393-0 2004 Upregulation of NAD(P)H oxidase 1 in hypoxia activates hypoxia-inducible factor 1 via increase in reactive oxygen species. Reactive Oxygen Species 98-121 NADPH oxidase 1 Homo sapiens 16-33 15817678-2 2005 Here, we show RANKL stimulation of BMM cells transiently increased the intracellular level of reactive oxygen species (ROS) through a signaling cascade involving TNF (tumor necrosis factor) receptor-associated factor (TRAF) 6, Rac1, and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (Nox) 1. Reactive Oxygen Species 119-122 NADPH oxidase 1 Homo sapiens 244-304 15817678-5 2005 Moreover, both RANKL-mediated ROS production and osteoclast differentiation were completely blocked in precursors depleted of Nox1 activity by RNA interference or by expressing a dominant-negative mutant of Rac1. Reactive Oxygen Species 30-33 NADPH oxidase 1 Homo sapiens 126-130 16083877-2 2005 Herein, P-gp and HIF-1alpha expression were investigated in multicellular prostate tumor spheroids overexpressing the ROS-generating enzyme Nox-1 in comparison to the mother cell line DU-145. Reactive Oxygen Species 118-121 NADPH oxidase 1 Homo sapiens 140-145 16083877-3 2005 In Nox-1-overexpressing tumor spheroids (DU-145Nox1) generation of ROS as well as expression of Nox-1 was significantly increased as compared to DU-145 tumor spheroids. Reactive Oxygen Species 67-70 NADPH oxidase 1 Homo sapiens 3-8 15817678-2 2005 Here, we show RANKL stimulation of BMM cells transiently increased the intracellular level of reactive oxygen species (ROS) through a signaling cascade involving TNF (tumor necrosis factor) receptor-associated factor (TRAF) 6, Rac1, and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (Nox) 1. Reactive Oxygen Species 94-117 NADPH oxidase 1 Homo sapiens 244-304 15110393-4 2004 Upregulation of Nox1 mRNA and protein occurred during hypoxia, accompanied by enhanced reactive oxygen species (ROS) generation. Reactive Oxygen Species 87-110 NADPH oxidase 1 Homo sapiens 16-20 15110393-4 2004 Upregulation of Nox1 mRNA and protein occurred during hypoxia, accompanied by enhanced reactive oxygen species (ROS) generation. Reactive Oxygen Species 112-115 NADPH oxidase 1 Homo sapiens 16-20 15110393-5 2004 A549 cells, which were transfected with a Nox1 expression vector, revealed an increase in ROS generation accompanied by activation of HIF-1-dependent target gene expression (heme oxygenase 1 mRNA, hypoxia-responsive-element reporter gene activity). Reactive Oxygen Species 90-93 NADPH oxidase 1 Homo sapiens 42-46 15121857-5 2004 Moreover, the depletion of Nox1 by RNA interference inhibited growth factor-induced ROS generation. Reactive Oxygen Species 84-87 NADPH oxidase 1 Homo sapiens 27-31 15150115-5 2004 Therefore, we propose that increased reactive oxygen species generation by Ras-induced Nox1 is required for oncogenic Ras transformation. Reactive Oxygen Species 37-60 NADPH oxidase 1 Homo sapiens 87-91 15121857-6 2004 These results suggest that ROS production in growth factor-stimulated cells is mediated by the sequential activation of PI3K, beta Pix, and Rac1, which then binds to Nox1 to stimulate its NADPH oxidase activity. Reactive Oxygen Species 27-30 NADPH oxidase 1 Homo sapiens 166-170 12817011-2 2003 We studied the expression and function of a recently described source of ROS, NAD(P)H oxidase 1 or Nox1, which has been associated with cell proliferation. Reactive Oxygen Species 73-76 NADPH oxidase 1 Homo sapiens 78-95 14670934-2 2004 Nox1 and Nox4, two homologues to the phagocytic NAD(P)H subunit gp91phox, both generate ROS in VSMC but differ in their response to growth factors. Reactive Oxygen Species 88-91 NADPH oxidase 1 Homo sapiens 0-4 14617635-4 2004 Co-transfection of Nox1, NOXO1, and NOXA1 reconstitutes ROS (reactive oxygen species) generation in HEK293 cells in the absence of cell stimulation. Reactive Oxygen Species 56-59 NADPH oxidase 1 Homo sapiens 19-23 14617635-4 2004 Co-transfection of Nox1, NOXO1, and NOXA1 reconstitutes ROS (reactive oxygen species) generation in HEK293 cells in the absence of cell stimulation. Reactive Oxygen Species 61-84 NADPH oxidase 1 Homo sapiens 19-23 11331784-2 2001 This study explores the role of reactive oxygen species (ROS) in regulating cell growth and transformation by Nox1. Reactive Oxygen Species 32-55 NADPH oxidase 1 Homo sapiens 110-114 11331784-2 2001 This study explores the role of reactive oxygen species (ROS) in regulating cell growth and transformation by Nox1. Reactive Oxygen Species 57-60 NADPH oxidase 1 Homo sapiens 110-114 34369274-0 2021 Transferrin receptor-mediated reactive oxygen species promotes ferroptosis of KGN cells via regulating NADPH oxidase 1/PTEN induced kinase 1/acyl-CoA synthetase long chain family member 4 signaling. Reactive Oxygen Species 30-53 NADPH oxidase 1 Homo sapiens 103-118 34338093-6 2021 The use of inhibitors demonstrated that endocytosis of these MV by VSMC led to a signaling cascade in the cytoplasm beginning with ERK1/2 signaling, then increased (Ca2+)i and stimulation of ROS production, mediated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)1/4. Reactive Oxygen Species 191-194 NADPH oxidase 1 Homo sapiens 219-287 34369274-11 2021 Iron uptake mediated the activation of NADPH oxidase 1 (NOX1) signaling, which induced the release of reactive oxygen species (ROS) and mitochondrial damage. Reactive Oxygen Species 127-130 NADPH oxidase 1 Homo sapiens 39-54 34369274-11 2021 Iron uptake mediated the activation of NADPH oxidase 1 (NOX1) signaling, which induced the release of reactive oxygen species (ROS) and mitochondrial damage. Reactive Oxygen Species 127-130 NADPH oxidase 1 Homo sapiens 56-60 34338093-9 2021 CONCLUSION: We conclude that endocytosis of pro-mineralizing MV can induce a series of signaling events in normal VSMC that culminate in generation of ROS via activation of NOX1/4. Reactive Oxygen Species 151-154 NADPH oxidase 1 Homo sapiens 173-179 35199405-4 2022 Micro-organisms, organelles and enzymes play crucial role in ROS generation, where NOX1 is the main intestinal enzyme, which produce ROS in the intestine epithelial cells. Reactive Oxygen Species 61-64 NADPH oxidase 1 Homo sapiens 83-87 35199405-4 2022 Micro-organisms, organelles and enzymes play crucial role in ROS generation, where NOX1 is the main intestinal enzyme, which produce ROS in the intestine epithelial cells. Reactive Oxygen Species 133-136 NADPH oxidase 1 Homo sapiens 83-87 35418176-6 2022 Mechanistically, OPN induced ROS production in HCC cells by upregulating the expression of NADPH oxidase 1 (NOX1). Reactive Oxygen Species 29-32 NADPH oxidase 1 Homo sapiens 91-106 35418176-0 2022 Osteopontin promotes hepatocellular carcinoma progression through inducing JAK2/STAT3/NOX1-mediated ROS production. Reactive Oxygen Species 100-103 NADPH oxidase 1 Homo sapiens 86-90 35418176-6 2022 Mechanistically, OPN induced ROS production in HCC cells by upregulating the expression of NADPH oxidase 1 (NOX1). Reactive Oxygen Species 29-32 NADPH oxidase 1 Homo sapiens 108-112 35418176-9 2022 In addition, NOX1 overexpression increased JAK2 and STAT3 phosphorylation by increasing ROS production, creating a positive feedback loop for stimulating JAK2/STAT3 signaling induced by OPN. Reactive Oxygen Species 88-91 NADPH oxidase 1 Homo sapiens 13-17 35274135-9 2022 Furthermore, the OPG-SDC-1 interaction increased reactive oxygen species (ROS) production through NOX1/4 activation. Reactive Oxygen Species 49-72 NADPH oxidase 1 Homo sapiens 98-104 35274135-9 2022 Furthermore, the OPG-SDC-1 interaction increased reactive oxygen species (ROS) production through NOX1/4 activation. Reactive Oxygen Species 74-77 NADPH oxidase 1 Homo sapiens 98-104 35274135-11 2022 In vascular smooth muscle cells (VSMCs), the OPG-SDC-1 interaction increased ROS production through NOX1/4 activation, subsequently increased MLC phosphorylation-mediated Rho kinase-MYPT1 regulation, leading to increased vascular contraction. Reactive Oxygen Species 77-80 NADPH oxidase 1 Homo sapiens 100-106 35085755-14 2022 Exposure to CM for 48h significantly enhanced intracellular HUVECs ROS production and this increase was prevented by the dual pharmacological inhibition of NOX1 and NOX2. Reactive Oxygen Species 67-70 NADPH oxidase 1 Homo sapiens 156-160 35085755-5 2022 In EC, ROS are mainly produced by NAPDH oxidases (NOX) such as NOX1 and NOX2. Reactive Oxygen Species 7-10 NADPH oxidase 1 Homo sapiens 63-67