PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33486699-3 2021 While NADPH oxidase (NOX2) is the major producer of ROS, transcription factor Nrf2 that induces antioxidant enzymes promotes efficient ROS disposal. Reactive Oxygen Species 52-55 cytochrome b-245, beta polypeptide Mus musculus 21-25 34055081-3 2021 NADPH oxidase s2 (NOX2) is a complex membrane protein that contributes to the production of reactive oxygen species (ROS) in several neurological diseases. Reactive Oxygen Species 92-115 cytochrome b-245, beta polypeptide Mus musculus 0-16 34055081-3 2021 NADPH oxidase s2 (NOX2) is a complex membrane protein that contributes to the production of reactive oxygen species (ROS) in several neurological diseases. Reactive Oxygen Species 92-115 cytochrome b-245, beta polypeptide Mus musculus 18-22 34055081-3 2021 NADPH oxidase s2 (NOX2) is a complex membrane protein that contributes to the production of reactive oxygen species (ROS) in several neurological diseases. Reactive Oxygen Species 117-120 cytochrome b-245, beta polypeptide Mus musculus 0-16 34055081-3 2021 NADPH oxidase s2 (NOX2) is a complex membrane protein that contributes to the production of reactive oxygen species (ROS) in several neurological diseases. Reactive Oxygen Species 117-120 cytochrome b-245, beta polypeptide Mus musculus 18-22 33691478-5 2021 Shear-enhanced ROS generation and activation of p47phox, an important regulatory subunit of NOX2, were diminished by the integrin antagonist integrilin or beta3 knockout, and by Galpha13 knockout or blocking the Galpha13-beta3 interaction. Reactive Oxygen Species 15-18 cytochrome b-245, beta polypeptide Mus musculus 92-96 33691478-9 2021 Importantly, NOX2-knockout platelets showed defective ROS generation, reduced platelet spreading without shear, and reduced platelet adhesion and thrombus volume on collagen and VWF (von Willibrand factor) under shear, whereas ROS inhibition diminished activation of tyrosine kinase Syk. Reactive Oxygen Species 54-57 cytochrome b-245, beta polypeptide Mus musculus 13-17 33691478-9 2021 Importantly, NOX2-knockout platelets showed defective ROS generation, reduced platelet spreading without shear, and reduced platelet adhesion and thrombus volume on collagen and VWF (von Willibrand factor) under shear, whereas ROS inhibition diminished activation of tyrosine kinase Syk. Reactive Oxygen Species 227-230 cytochrome b-245, beta polypeptide Mus musculus 13-17 33691478-10 2021 CONCLUSIONS: Outside-in signaling activates the mainly NOX2-mediated ROS generation, which mediates Syk-dependent secondary platelet activation, adhesion, and thrombosis with minimal effect on hemostasis. Reactive Oxygen Species 69-72 cytochrome b-245, beta polypeptide Mus musculus 55-59 33600816-4 2021 The effect of oxidative stress on the regulation of HAX-1 was examined using knockout mice lacking nicotinamide-adenine dinucleotide phosphate oxidase 2 (NOX2), which is a major source of reactive oxygen species (ROS) after cerebral ischemia. Reactive Oxygen Species 188-211 cytochrome b-245, beta polypeptide Mus musculus 99-152 33600816-4 2021 The effect of oxidative stress on the regulation of HAX-1 was examined using knockout mice lacking nicotinamide-adenine dinucleotide phosphate oxidase 2 (NOX2), which is a major source of reactive oxygen species (ROS) after cerebral ischemia. Reactive Oxygen Species 188-211 cytochrome b-245, beta polypeptide Mus musculus 154-158 33600816-4 2021 The effect of oxidative stress on the regulation of HAX-1 was examined using knockout mice lacking nicotinamide-adenine dinucleotide phosphate oxidase 2 (NOX2), which is a major source of reactive oxygen species (ROS) after cerebral ischemia. Reactive Oxygen Species 213-216 cytochrome b-245, beta polypeptide Mus musculus 99-152 33600816-10 2021 These findings suggest that HAX-1 has a neuroprotective effect against ischemic neuronal injury, and downregulation of HAX-1 by NOX2-produced ROS induces apoptosis after cerebral ischemia. Reactive Oxygen Species 142-145 cytochrome b-245, beta polypeptide Mus musculus 128-132 33486699-3 2021 While NADPH oxidase (NOX2) is the major producer of ROS, transcription factor Nrf2 that induces antioxidant enzymes promotes efficient ROS disposal. Reactive Oxygen Species 135-138 cytochrome b-245, beta polypeptide Mus musculus 21-25 32506037-10 2020 Our findings support a model in which Nox4 ROS induces RyR1 Ca2+ leak and the increased junctional space [Ca2+] exacerbates Nox2 ROS; with the cumulative effect of disruption of downstream cellular processes that would ultimately contribute to reduced muscle or cellular performance. Reactive Oxygen Species 129-132 cytochrome b-245, beta polypeptide Mus musculus 124-128 33187846-0 2021 Tetrachlorobenzoquinone exhibits immunotoxicity by inducing neutrophil extracellular traps through a mechanism involving ROS-JNK-NOX2 positive feedback loop. Reactive Oxygen Species 121-124 cytochrome b-245, beta polypeptide Mus musculus 129-133 33187846-8 2021 Mechanistically, JNK activation enhanced the expression of NADPH oxidase enzyme 2 (NOX2), which further accelerated the generation of ROS and thus amplified the formation of NETs. Reactive Oxygen Species 134-137 cytochrome b-245, beta polypeptide Mus musculus 59-81 33187846-8 2021 Mechanistically, JNK activation enhanced the expression of NADPH oxidase enzyme 2 (NOX2), which further accelerated the generation of ROS and thus amplified the formation of NETs. Reactive Oxygen Species 134-137 cytochrome b-245, beta polypeptide Mus musculus 83-87 33187846-9 2021 The pharmacologic blockage of JNK or NOX2 effectively ameliorated TCBQ-induced ROS and NETs, implying that ROS-JNK-NOX2 positive feedback loop was involved in TCBQ-induced NETs. Reactive Oxygen Species 79-82 cytochrome b-245, beta polypeptide Mus musculus 37-41 33187846-9 2021 The pharmacologic blockage of JNK or NOX2 effectively ameliorated TCBQ-induced ROS and NETs, implying that ROS-JNK-NOX2 positive feedback loop was involved in TCBQ-induced NETs. Reactive Oxygen Species 79-82 cytochrome b-245, beta polypeptide Mus musculus 115-119 33187846-9 2021 The pharmacologic blockage of JNK or NOX2 effectively ameliorated TCBQ-induced ROS and NETs, implying that ROS-JNK-NOX2 positive feedback loop was involved in TCBQ-induced NETs. Reactive Oxygen Species 107-110 cytochrome b-245, beta polypeptide Mus musculus 37-41 33187846-9 2021 The pharmacologic blockage of JNK or NOX2 effectively ameliorated TCBQ-induced ROS and NETs, implying that ROS-JNK-NOX2 positive feedback loop was involved in TCBQ-induced NETs. Reactive Oxygen Species 107-110 cytochrome b-245, beta polypeptide Mus musculus 115-119 33613105-10 2021 Furthermore, in macrophage cell lines and primary bone marrow- derived macrophages (BMDMs), beta-glucan-induced trained immunity can increase ROS production by activating NOX2 to promote macrophage LAP. Reactive Oxygen Species 142-145 cytochrome b-245, beta polypeptide Mus musculus 171-175 32967913-0 2020 Idelalisib rescues natural killer cells from monocyte-induced immunosuppression by inhibiting NOX2-derived reactive oxygen species. Reactive Oxygen Species 107-130 cytochrome b-245, beta polypeptide Mus musculus 94-98 32967913-2 2020 PI3K regulates the formation of reactive oxygen species (ROS) by the myeloid NADPH oxidase NOX2, but the role of PI3Kdelta in myeloid cell-induced immunosuppression is unexplored. Reactive Oxygen Species 32-55 cytochrome b-245, beta polypeptide Mus musculus 91-95 32967913-2 2020 PI3K regulates the formation of reactive oxygen species (ROS) by the myeloid NADPH oxidase NOX2, but the role of PI3Kdelta in myeloid cell-induced immunosuppression is unexplored. Reactive Oxygen Species 57-60 cytochrome b-245, beta polypeptide Mus musculus 91-95 32967913-4 2020 Idelalisib potently and efficiently inhibited the formation of NOX2-derived ROS from monocytes and rescued NK cells from ROS-induced cell death. Reactive Oxygen Species 76-79 cytochrome b-245, beta polypeptide Mus musculus 63-67 33114493-4 2020 METHODS AND RESULTS: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Reactive Oxygen Species 66-69 cytochrome b-245, beta polypeptide Mus musculus 38-42 33114493-4 2020 METHODS AND RESULTS: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Reactive Oxygen Species 66-69 cytochrome b-245, beta polypeptide Mus musculus 158-162 33039662-12 2021 Overall, these data suggest an important role for Hv1 in regulating tissue acidosis, NOX2-mediated ROS production, and functional outcome following SCI. Reactive Oxygen Species 99-102 cytochrome b-245, beta polypeptide Mus musculus 85-89 33391487-14 2021 Conclusions: MPO and NOX2 are the dominant sources of ROS/RNS in acute and chronic DTHR. Reactive Oxygen Species 54-57 cytochrome b-245, beta polypeptide Mus musculus 21-25 32209423-6 2020 HuA considerably decreased ROS levels by downregulating the high levels of NADPH oxidase (NOX 2, NOX 4) mediated by CIH. Reactive Oxygen Species 27-30 cytochrome b-245, beta polypeptide Mus musculus 90-95 32129097-5 2020 This was concomitant with sustained oxidative stress from the overactivation of NADPH oxidase 2, a major intracellular source of reactive oxygen species, in both the cell types. Reactive Oxygen Species 129-152 cytochrome b-245, beta polypeptide Mus musculus 80-95 32507594-8 2020 Increased ROS production measured in HFD heart homogenates was inhibited to control levels by Tiron (a cell membrane permeable O2 -scavenger), diphenyleneiodonium (DPI, a flavohaemoprotein inhibitor) and Nox2 ds-tat (a Nox2 assembly inhibitor). Reactive Oxygen Species 10-13 cytochrome b-245, beta polypeptide Mus musculus 204-208 32507594-8 2020 Increased ROS production measured in HFD heart homogenates was inhibited to control levels by Tiron (a cell membrane permeable O2 -scavenger), diphenyleneiodonium (DPI, a flavohaemoprotein inhibitor) and Nox2 ds-tat (a Nox2 assembly inhibitor). Reactive Oxygen Species 10-13 cytochrome b-245, beta polypeptide Mus musculus 219-223 32635630-7 2020 A local significantly increased ROS production was also found in Nox2 and Nox4 knockout mice but not in Nox1 knockout mice who further had significantly lower systemic oxidative stress and DNA damage than WT animals. Reactive Oxygen Species 32-35 cytochrome b-245, beta polypeptide Mus musculus 65-69 31980577-8 2020 LETMD1 attenuation also enhanced LPS-induced expression of NADPH oxidase (NOX) 2, the main producer of cellular ROS in phagocytes, through augmenting IFN regulatory factor 1. Reactive Oxygen Species 112-115 cytochrome b-245, beta polypeptide Mus musculus 59-80 32397166-11 2020 Furthermore, hyperglycemia induced NOX2 expression and ROS production through the HG/miR-21/PI3K/NOX2/ROS signaling cascade. Reactive Oxygen Species 55-58 cytochrome b-245, beta polypeptide Mus musculus 97-101 32397166-11 2020 Furthermore, hyperglycemia induced NOX2 expression and ROS production through the HG/miR-21/PI3K/NOX2/ROS signaling cascade. Reactive Oxygen Species 102-105 cytochrome b-245, beta polypeptide Mus musculus 35-39 32397166-11 2020 Furthermore, hyperglycemia induced NOX2 expression and ROS production through the HG/miR-21/PI3K/NOX2/ROS signaling cascade. Reactive Oxygen Species 102-105 cytochrome b-245, beta polypeptide Mus musculus 97-101 31667656-7 2020 Our results show that pilocarpine induced NOX2 activation to produce ROS in mice brain and that administration of ketamine before or after the induction of temporal lobe epilepsy by pilocarpine inhibited this activation in mice brain. Reactive Oxygen Species 69-72 cytochrome b-245, beta polypeptide Mus musculus 42-46 32160269-4 2020 We used C57BL/6 (WT) and a gp91PHOX knockout mice (PHOX-/-), lacking functional NOX2, to investigate the effects of ablation of NOX2-derived ROS production on the outcome of acute chagasic cardiomyopathy. Reactive Oxygen Species 141-144 cytochrome b-245, beta polypeptide Mus musculus 128-132 32160269-11 2020 Overall our data show for the first time that lack of NOX2-derived ROS promoted a pro-arrhythmic phenotype in the heart, in which the crosstalk between ROS and NO could play an important role in regulating cardiomyocyte electro-mechanical function during acute CD. Reactive Oxygen Species 67-70 cytochrome b-245, beta polypeptide Mus musculus 54-58 32160269-11 2020 Overall our data show for the first time that lack of NOX2-derived ROS promoted a pro-arrhythmic phenotype in the heart, in which the crosstalk between ROS and NO could play an important role in regulating cardiomyocyte electro-mechanical function during acute CD. Reactive Oxygen Species 152-155 cytochrome b-245, beta polypeptide Mus musculus 54-58 32160269-12 2020 Future studies designed to evaluate the potential role of NOX2-derived ROS in the chronic phase of CD could open new and more specific therapeutic strategies to treat CD and prevent deaths due to heart complications. Reactive Oxygen Species 71-74 cytochrome b-245, beta polypeptide Mus musculus 58-62 32005915-1 2020 Microglia express constitutively a Nox2 enzyme that is involved in neuroinflammation by the generation of reactive oxygen species (ROS). Reactive Oxygen Species 106-129 cytochrome b-245, beta polypeptide Mus musculus 35-39 32116666-9 2019 HBN normalized ROS over-production of NOX2 and nitrotyrosine, reversed the reduction of anti-oxidant marker, SOD-1 as well as restored NO bioavailability in both HUVECs challenged with HG and in db/db diabetic mice. Reactive Oxygen Species 15-18 cytochrome b-245, beta polypeptide Mus musculus 38-42 32093119-3 2020 One of the major ROS-generating enzymes in the cardiomyocytes is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), and many potential systemic activators of NOX2 are elevated in obesity and diabetes. Reactive Oxygen Species 17-20 cytochrome b-245, beta polypeptide Mus musculus 65-126 32093119-3 2020 One of the major ROS-generating enzymes in the cardiomyocytes is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), and many potential systemic activators of NOX2 are elevated in obesity and diabetes. Reactive Oxygen Species 17-20 cytochrome b-245, beta polypeptide Mus musculus 128-132 32093119-3 2020 One of the major ROS-generating enzymes in the cardiomyocytes is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), and many potential systemic activators of NOX2 are elevated in obesity and diabetes. Reactive Oxygen Species 17-20 cytochrome b-245, beta polypeptide Mus musculus 177-181 32093119-8 2020 Mitochondrial ROS production was also reduced following NOX2 inhibition, while cardiac mitochondrial function was not markedly altered by apocynin-treatment. Reactive Oxygen Species 14-17 cytochrome b-245, beta polypeptide Mus musculus 56-60 32005915-1 2020 Microglia express constitutively a Nox2 enzyme that is involved in neuroinflammation by the generation of reactive oxygen species (ROS). Reactive Oxygen Species 131-134 cytochrome b-245, beta polypeptide Mus musculus 35-39 32005915-7 2020 Compared to young (3-4 months) controls, midbrain tissues from wild-type aging mice (20-22 months) had significantly higher levels of Nox2-derived ROS production, Abeta deposition, microgliosis and IL-1beta production. Reactive Oxygen Species 147-150 cytochrome b-245, beta polypeptide Mus musculus 134-138 33099296-6 2020 A recent study showed that activation of NOX might aggravate the primary TBI, and among these members, NOX2 is the key member in regulation of uncontrolled ROS expression, and thus plays a critical role in development of inflammatory diseases. Reactive Oxygen Species 156-159 cytochrome b-245, beta polypeptide Mus musculus 103-107 31604916-0 2019 Cytosolic ROS production by NADPH oxidase 2 regulates muscle glucose uptake during exercise. Reactive Oxygen Species 10-13 cytochrome b-245, beta polypeptide Mus musculus 28-43 31604916-3 2019 Here, we combined exercise in humans and mice with fluorescent dyes, genetically-encoded biosensors, and NADPH oxidase 2 (NOX2) loss-of-function models to demonstrate that NOX2 is the main source of cytosolic ROS during moderate-intensity exercise in skeletal muscle. Reactive Oxygen Species 209-212 cytochrome b-245, beta polypeptide Mus musculus 172-176 31604916-5 2019 These findings indicate that NOX2 is a major myocellular ROS source, regulating glucose transport capacity during moderate-intensity exercise. Reactive Oxygen Species 57-60 cytochrome b-245, beta polypeptide Mus musculus 29-33 31349119-1 2019 The phagocyte NADPH oxidase (the NOX2 complex) generates superoxide, the precursor to reactive oxygen species (ROS). Reactive Oxygen Species 86-109 cytochrome b-245, beta polypeptide Mus musculus 33-37 31349119-1 2019 The phagocyte NADPH oxidase (the NOX2 complex) generates superoxide, the precursor to reactive oxygen species (ROS). Reactive Oxygen Species 111-114 cytochrome b-245, beta polypeptide Mus musculus 33-37 31349119-11 2019 We deduce that the inflammatory rerouting of immune-stimulatory necrotic material into inflammatory phagocyte subsets contributes to the connection between low ROS production by the NOX2 complex and SLE. Reactive Oxygen Species 160-163 cytochrome b-245, beta polypeptide Mus musculus 182-186 31308397-6 2019 Moreover, we found that ROS production was dependent on the NOX2 phagocyte NADPH oxidase. Reactive Oxygen Species 24-27 cytochrome b-245, beta polypeptide Mus musculus 60-64 31176685-3 2019 Analysis of the expressions of NADPH oxidases (NOXs) and dual oxidases, crucial enzymes involved in intracellular ROS formation, shows NOX2/gp91phox is over-expressed in p38alpha deficient cells. Reactive Oxygen Species 114-117 cytochrome b-245, beta polypeptide Mus musculus 135-139 31176685-3 2019 Analysis of the expressions of NADPH oxidases (NOXs) and dual oxidases, crucial enzymes involved in intracellular ROS formation, shows NOX2/gp91phox is over-expressed in p38alpha deficient cells. Reactive Oxygen Species 114-117 cytochrome b-245, beta polypeptide Mus musculus 140-148 31176685-5 2019 ROS formation decreased when the level of NOX2 was silenced by siRNA in p38alpha deficient cells. Reactive Oxygen Species 0-3 cytochrome b-245, beta polypeptide Mus musculus 42-46 30807841-1 2019 NADPH oxidase (NOX2) is an enzyme that induces reactive oxygen species (ROS) and serves as a switch between the pro-inflammatory and neurorestorative microglial/macrophage phenotypes; such changes play an important role in neuropathic pain and motor dysfunction. Reactive Oxygen Species 47-70 cytochrome b-245, beta polypeptide Mus musculus 15-19 30807841-1 2019 NADPH oxidase (NOX2) is an enzyme that induces reactive oxygen species (ROS) and serves as a switch between the pro-inflammatory and neurorestorative microglial/macrophage phenotypes; such changes play an important role in neuropathic pain and motor dysfunction. Reactive Oxygen Species 72-75 cytochrome b-245, beta polypeptide Mus musculus 15-19 30807841-6 2019 Deletion of NOX2 significantly reduced CD11b+/CD45hiF4/80+ macrophage infiltration at 24 h post-injury detected by flow cytometry and 8-OHG+ ROS production at 8 weeks post-injury by IHC in both lesion area and lumbar enlargement. Reactive Oxygen Species 141-144 cytochrome b-245, beta polypeptide Mus musculus 12-16 30995916-13 2019 During the subsequent inflammatory response to excitotoxic damage, ROS generated by NOX-2 play a decisive role in the extension of the lesion and consequently in the severity of the functional compromise, probably by regulating the anti-inflammatory cytokines production. Reactive Oxygen Species 67-70 cytochrome b-245, beta polypeptide Mus musculus 84-89 31146911-7 2019 CONCLUSION: In APP/PS1 mice, macrophage-derived CXCL1 can promote the proliferation of neural stem cells in the subventricular zone via the NOX2-ROS-PI3K/Akt pathway. Reactive Oxygen Species 145-148 cytochrome b-245, beta polypeptide Mus musculus 140-144 31338092-3 2019 Previous studies in our laboratory using a murine model of SIRS demonstrated a key role for NADPH oxidase 2 (Nox2)-derived reactive oxygen species in the resolution of inflammation. Reactive Oxygen Species 123-146 cytochrome b-245, beta polypeptide Mus musculus 92-107 31338092-3 2019 Previous studies in our laboratory using a murine model of SIRS demonstrated a key role for NADPH oxidase 2 (Nox2)-derived reactive oxygen species in the resolution of inflammation. Reactive Oxygen Species 123-146 cytochrome b-245, beta polypeptide Mus musculus 109-113 31118934-2 2019 Ablation of ROS derived from phagocytic NADPH oxidase 2 is protective against autoimmune diabetes in non-obese diabetic (NOD) mice. Reactive Oxygen Species 12-15 cytochrome b-245, beta polypeptide Mus musculus 40-55 31118934-3 2019 However, the mechanisms of NADPH oxidase 2-derived ROS in T1D pathogenesis need to be elucidated. Reactive Oxygen Species 51-54 cytochrome b-245, beta polypeptide Mus musculus 27-42 30051353-9 2019 Mechanistic studies revealed that increase in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-2 (NOX2)-dependent superoxide/reactive oxygen species (ROS) production plays a key role in both LPS- and DSP-4-elicited neurotoxicity. Reactive Oxygen Species 136-159 cytochrome b-245, beta polypeptide Mus musculus 46-107 30051353-9 2019 Mechanistic studies revealed that increase in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-2 (NOX2)-dependent superoxide/reactive oxygen species (ROS) production plays a key role in both LPS- and DSP-4-elicited neurotoxicity. Reactive Oxygen Species 136-159 cytochrome b-245, beta polypeptide Mus musculus 109-113 30342191-9 2018 Pharmacological inhibition of Nox2 decreased reactive oxygen species production and protein oxidative modifications in the muscle of ApoE-/- mice subjected to a Western-type diet. Reactive Oxygen Species 45-68 cytochrome b-245, beta polypeptide Mus musculus 30-34 30288635-2 2019 Reactive oxygen species (ROS), produced in part by the neutrophil NADPH oxidase 2 (Nox2), have been implicated in the pathogenesis of ALI. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 66-81 30288635-2 2019 Reactive oxygen species (ROS), produced in part by the neutrophil NADPH oxidase 2 (Nox2), have been implicated in the pathogenesis of ALI. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 83-87 30323311-9 2019 We propose that NOX2-derived ROS may contribute to the progression of KRAS-induced leukemia and that strategies to target NOX2 merit further evaluation in RAS-mutated hematopoietic cancer. Reactive Oxygen Species 29-32 cytochrome b-245, beta polypeptide Mus musculus 16-20 30897521-3 2019 We postulated that TNFalpha-induced endothelial reactive oxygen species (ROS) generation and pro-inflammatory signaling would be ameliorated by targeting Nox2. Reactive Oxygen Species 48-71 cytochrome b-245, beta polypeptide Mus musculus 154-158 30897521-3 2019 We postulated that TNFalpha-induced endothelial reactive oxygen species (ROS) generation and pro-inflammatory signaling would be ameliorated by targeting Nox2. Reactive Oxygen Species 73-76 cytochrome b-245, beta polypeptide Mus musculus 154-158 30315349-1 2019 Myeloid-derived suppressor cells (MDSCs) are immature monocytes and granulocytes that impede immune-mediated clearance of malignant cells by multiple mechanisms, including the formation of immunosuppressive reactive oxygen species (ROS) via the myeloid cell NADPH oxidase (NOX2). Reactive Oxygen Species 207-230 cytochrome b-245, beta polypeptide Mus musculus 273-277 30315349-1 2019 Myeloid-derived suppressor cells (MDSCs) are immature monocytes and granulocytes that impede immune-mediated clearance of malignant cells by multiple mechanisms, including the formation of immunosuppressive reactive oxygen species (ROS) via the myeloid cell NADPH oxidase (NOX2). Reactive Oxygen Species 232-235 cytochrome b-245, beta polypeptide Mus musculus 273-277 30288635-2 2019 Reactive oxygen species (ROS), produced in part by the neutrophil NADPH oxidase 2 (Nox2), have been implicated in the pathogenesis of ALI. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 66-81 30288635-2 2019 Reactive oxygen species (ROS), produced in part by the neutrophil NADPH oxidase 2 (Nox2), have been implicated in the pathogenesis of ALI. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 83-87 29083257-2 2018 Surprisingly, both NADPH oxidase 2 (NOX2) that increases and transcription factor Nrf2 that decreases reactive oxygen species (ROS) are induced after TBI. Reactive Oxygen Species 102-125 cytochrome b-245, beta polypeptide Mus musculus 36-40 30195046-2 2018 S100A8/A9 can induce reactive oxygen species (ROS) release by phagocytes in OA synovium via neutrophil cytosolic factor-1 (Ncf1)-regulated NOX2 activation. Reactive Oxygen Species 46-49 cytochrome b-245, beta polypeptide Mus musculus 139-143 30195046-3 2018 In the present study we investigated whether NOX2-derived ROS affect joint pathology during CiOA. Reactive Oxygen Species 58-61 cytochrome b-245, beta polypeptide Mus musculus 45-49 29897791-11 2018 To support the importance of Rac2 in the macrophage immune response, overexpression of constitutively active Rac2 by lentiviral administration increased NOX2-derived ROS, decreased bacterial burden in lung tissue, and increased survival compared with CS-exposed control mice. Reactive Oxygen Species 166-169 cytochrome b-245, beta polypeptide Mus musculus 153-157 30347077-1 2018 Purpose: Oxidative stress plays a central role in the development of diabetic retinopathy, and in the pathogenesis of this blinding disease, activation of NADPH oxidase 2 (Nox2)-mediated cytosolic reactive oxygen species (ROS) production precedes mitochondrial damage. Reactive Oxygen Species 197-220 cytochrome b-245, beta polypeptide Mus musculus 155-170 30347077-1 2018 Purpose: Oxidative stress plays a central role in the development of diabetic retinopathy, and in the pathogenesis of this blinding disease, activation of NADPH oxidase 2 (Nox2)-mediated cytosolic reactive oxygen species (ROS) production precedes mitochondrial damage. Reactive Oxygen Species 197-220 cytochrome b-245, beta polypeptide Mus musculus 172-176 30347077-1 2018 Purpose: Oxidative stress plays a central role in the development of diabetic retinopathy, and in the pathogenesis of this blinding disease, activation of NADPH oxidase 2 (Nox2)-mediated cytosolic reactive oxygen species (ROS) production precedes mitochondrial damage. Reactive Oxygen Species 222-225 cytochrome b-245, beta polypeptide Mus musculus 155-170 30347077-1 2018 Purpose: Oxidative stress plays a central role in the development of diabetic retinopathy, and in the pathogenesis of this blinding disease, activation of NADPH oxidase 2 (Nox2)-mediated cytosolic reactive oxygen species (ROS) production precedes mitochondrial damage. Reactive Oxygen Species 222-225 cytochrome b-245, beta polypeptide Mus musculus 172-176 30195046-0 2018 The role of NOX2-derived reactive oxygen species in collagenase-induced osteoarthritis. Reactive Oxygen Species 25-48 cytochrome b-245, beta polypeptide Mus musculus 12-16 30195046-2 2018 S100A8/A9 can induce reactive oxygen species (ROS) release by phagocytes in OA synovium via neutrophil cytosolic factor-1 (Ncf1)-regulated NOX2 activation. Reactive Oxygen Species 21-44 cytochrome b-245, beta polypeptide Mus musculus 139-143 29897791-4 2018 OBJECTIVES: Determine how cigarette smoke (CS) reduces reactive oxygen species (ROS) production by the phagocytic NOX2 (NADPH oxidase 2), which is essential for innate immunity in lung macrophages. Reactive Oxygen Species 55-78 cytochrome b-245, beta polypeptide Mus musculus 114-118 29897791-4 2018 OBJECTIVES: Determine how cigarette smoke (CS) reduces reactive oxygen species (ROS) production by the phagocytic NOX2 (NADPH oxidase 2), which is essential for innate immunity in lung macrophages. Reactive Oxygen Species 55-78 cytochrome b-245, beta polypeptide Mus musculus 120-135 29897791-4 2018 OBJECTIVES: Determine how cigarette smoke (CS) reduces reactive oxygen species (ROS) production by the phagocytic NOX2 (NADPH oxidase 2), which is essential for innate immunity in lung macrophages. Reactive Oxygen Species 80-83 cytochrome b-245, beta polypeptide Mus musculus 114-118 29897791-4 2018 OBJECTIVES: Determine how cigarette smoke (CS) reduces reactive oxygen species (ROS) production by the phagocytic NOX2 (NADPH oxidase 2), which is essential for innate immunity in lung macrophages. Reactive Oxygen Species 80-83 cytochrome b-245, beta polypeptide Mus musculus 120-135 29897791-5 2018 METHODS: NOX2-derived ROS and Rac2 (Ras-related C3 botulinum toxin substrate 2) activity were determined in BAL cells from wild-type and Rac2-/- mice exposed to CS or cadmium and in BAL cells from subjects that smoke. Reactive Oxygen Species 22-25 cytochrome b-245, beta polypeptide Mus musculus 9-13 29897791-7 2018 MEASUREMENTS AND MAIN RESULTS: NOX2-derived ROS in BAL cells was reduced in mice exposed to CS via inhibition of the small GTPase Rac2. Reactive Oxygen Species 44-47 cytochrome b-245, beta polypeptide Mus musculus 31-35 29083257-2 2018 Surprisingly, both NADPH oxidase 2 (NOX2) that increases and transcription factor Nrf2 that decreases reactive oxygen species (ROS) are induced after TBI. Reactive Oxygen Species 102-125 cytochrome b-245, beta polypeptide Mus musculus 19-34 29083257-2 2018 Surprisingly, both NADPH oxidase 2 (NOX2) that increases and transcription factor Nrf2 that decreases reactive oxygen species (ROS) are induced after TBI. Reactive Oxygen Species 127-130 cytochrome b-245, beta polypeptide Mus musculus 19-34 29083257-2 2018 Surprisingly, both NADPH oxidase 2 (NOX2) that increases and transcription factor Nrf2 that decreases reactive oxygen species (ROS) are induced after TBI. Reactive Oxygen Species 127-130 cytochrome b-245, beta polypeptide Mus musculus 36-40 29083257-4 2018 Genetic deletion of NOX2 improved, while Nrf2 worsened the post-TBI motor function recovery and lesion volume indicating that decreasing ROS levels might be beneficial after TBI. Reactive Oxygen Species 137-140 cytochrome b-245, beta polypeptide Mus musculus 20-24 30154263-5 2018 The absence of Nox1 or Nox2, gp91 subunit isoforms of the Nox complex, reversed ROS-mediated clearance of CTG parasites. Reactive Oxygen Species 80-83 cytochrome b-245, beta polypeptide Mus musculus 23-27 30007118-1 2018 Essentials Reactive oxygen species (ROS) generation by NOX2 plays a critical role in platelet activation. Reactive Oxygen Species 36-39 cytochrome b-245, beta polypeptide Mus musculus 55-59 30007118-5 2018 SUMMARY: Background Platelets from patients with X-linked chronic granulomatous disease or mice deficient in nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) oxidase isoform NOX2 exhibit diminished reactive oxygen species (ROS) generation and platelet activation. Reactive Oxygen Species 205-228 cytochrome b-245, beta polypeptide Mus musculus 181-185 30007118-5 2018 SUMMARY: Background Platelets from patients with X-linked chronic granulomatous disease or mice deficient in nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) oxidase isoform NOX2 exhibit diminished reactive oxygen species (ROS) generation and platelet activation. Reactive Oxygen Species 230-233 cytochrome b-245, beta polypeptide Mus musculus 181-185 30050527-1 2018 Chronic granulomatous disease (CGD) is a primary immunodeficiency resulting from loss of function mutations in the reactive oxygen species generating phagocyte NADPH oxidase (NOX2). Reactive Oxygen Species 115-138 cytochrome b-245, beta polypeptide Mus musculus 175-179 29625277-9 2018 CONCLUSION: The experimental results support that Pak1 stimulation can attenuate NCX-dependent Ca2+ overload and prevent triggered arrhythmic activity by suppressing NOX2-dependent ROS production. Reactive Oxygen Species 181-184 cytochrome b-245, beta polypeptide Mus musculus 166-170 29780806-3 2018 Previous studies suggest that reactive oxygen species, such as hydrogen peroxide (H2O2), produced from NADPH oxidase 2 play a critical role in platelet-neutrophil interactions by regulating the function of neutrophil alphaMbeta2 integrin during sterile inflammation. Reactive Oxygen Species 30-53 cytochrome b-245, beta polypeptide Mus musculus 103-118 29789380-3 2018 In visual cortical neurons, sustained synaptic stimulation activate the enzymatic complex NOX2, resulting in the generation of reactive oxygen species (ROS). Reactive Oxygen Species 127-150 cytochrome b-245, beta polypeptide Mus musculus 90-94 29789380-3 2018 In visual cortical neurons, sustained synaptic stimulation activate the enzymatic complex NOX2, resulting in the generation of reactive oxygen species (ROS). Reactive Oxygen Species 152-155 cytochrome b-245, beta polypeptide Mus musculus 90-94 29789380-10 2018 This process requires the production of reactive oxygen species mediated by the enzymatic complex NOX2. Reactive Oxygen Species 40-63 cytochrome b-245, beta polypeptide Mus musculus 98-102 29753328-5 2018 METHODS: To reduce NADPH oxidase 2-derived ROS production, mice with deficits of NOX regulatory subunit/NOX2 organizer p47phox (p47phox-/-) or NOX2 major subunit gp91phox (gp91phox-/-) were used or the NOX2-selective inhibitor diphenyleneiodonium (DPI) was used to treat wild-type (WT) mice. Reactive Oxygen Species 43-46 cytochrome b-245, beta polypeptide Mus musculus 19-34 28942245-5 2017 Delayed inhibition of NOX2, beginning one day after TBI, reduced reactive oxygen species production of myeloid cells and protected neurons from oxidative damage. Reactive Oxygen Species 65-88 cytochrome b-245, beta polypeptide Mus musculus 22-26 29761170-3 2018 Nicotinamide adenine dinucleotide phosphate (reduced) oxidase 2 (NOX2; also known as gp91Phox), the main catalytic subunit of the nicotinamide adenine dinucleotide phosphate (reduced) oxidase complex, modulates ROS production, immune responsiveness, and pathogenesis of obesity-associated metabolic derangements. Reactive Oxygen Species 211-214 cytochrome b-245, beta polypeptide Mus musculus 65-69 29761170-3 2018 Nicotinamide adenine dinucleotide phosphate (reduced) oxidase 2 (NOX2; also known as gp91Phox), the main catalytic subunit of the nicotinamide adenine dinucleotide phosphate (reduced) oxidase complex, modulates ROS production, immune responsiveness, and pathogenesis of obesity-associated metabolic derangements. Reactive Oxygen Species 211-214 cytochrome b-245, beta polypeptide Mus musculus 85-93 29761170-6 2018 Genetic ablation of NOX2 impeded immune cell ROS synthesis and was sufficient to uncouple obesity from glucose dysmetabolism and NAFLD pathogenesis. Reactive Oxygen Species 45-48 cytochrome b-245, beta polypeptide Mus musculus 20-24 29761170-8 2018 Conclusion: Current findings demonstrate a crucial role of the NOX2-ROS axis in immune cell effector function and polarization and consequent NAFLD progression in obesity. Reactive Oxygen Species 68-71 cytochrome b-245, beta polypeptide Mus musculus 63-67 28552746-7 2018 The production of reactive oxygen species (ROS) and the presence of proteins (nitrotyrosine, NOx-2 and NOx-4) involved in ROS generation were evaluated with dihydroethidium (DHE) fluorescence and by Western blotting, respectively. Reactive Oxygen Species 122-125 cytochrome b-245, beta polypeptide Mus musculus 93-98 29158417-9 2018 Provision of exogenous ROS in the form of H2O2 reversed the necrotic phenotype and restored CD95 expression on infected gp91phox-/- neutrophils. Reactive Oxygen Species 23-26 cytochrome b-245, beta polypeptide Mus musculus 120-128 28467721-10 2017 Our in vivo results point to a regulatory role of NOX2-derived ROS not only during priming but also during the effector phase of CIA, most likely via different mechanisms. Reactive Oxygen Species 63-66 cytochrome b-245, beta polypeptide Mus musculus 50-54 29731721-11 2018 AIP1 via its proline-rich region binds to the SH3 domain of cytosolic subunit p47phox to disrupt formation of an active NOX2 complex, attenuating ROS production. Reactive Oxygen Species 146-149 cytochrome b-245, beta polypeptide Mus musculus 120-124 29410242-15 2018 Ethanol-induced Ca2+-leak was abolished in mice with knockout of NOX2 (the main source for ROS in cardiomyocytes). Reactive Oxygen Species 91-94 cytochrome b-245, beta polypeptide Mus musculus 65-69 29410242-19 2018 Mechanistically, ROS-production via NOX2 and oxidative activation of CaMKII appear to play central roles. Reactive Oxygen Species 17-20 cytochrome b-245, beta polypeptide Mus musculus 36-40 29158417-0 2018 NOX2-Derived Reactive Oxygen Species Control Inflammation during Leishmania amazonensis Infection by Mediating Infection-Induced Neutrophil Apoptosis. Reactive Oxygen Species 13-36 cytochrome b-245, beta polypeptide Mus musculus 0-4 29158417-1 2018 Reactive oxygen species (ROS) produced by NADPH phagocyte oxidase isoform (NOX2) are critical for the elimination of intracellular pathogens in many infections. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 75-79 29158417-1 2018 Reactive oxygen species (ROS) produced by NADPH phagocyte oxidase isoform (NOX2) are critical for the elimination of intracellular pathogens in many infections. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 75-79 29158417-4 2018 Despite equivalent parasite loads compared with wild-type (WT) mice, mice deficient in ROS production by NOX2 due to the absence of the gp91 subunit (gp91phox-/-) had significantly more severe pathology in the later stages of infection. Reactive Oxygen Species 87-90 cytochrome b-245, beta polypeptide Mus musculus 105-109 29158417-4 2018 Despite equivalent parasite loads compared with wild-type (WT) mice, mice deficient in ROS production by NOX2 due to the absence of the gp91 subunit (gp91phox-/-) had significantly more severe pathology in the later stages of infection. Reactive Oxygen Species 87-90 cytochrome b-245, beta polypeptide Mus musculus 150-158 28467721-1 2017 AIMS: Neutrophil cytosolic factor 1 (NCF1) is a key regulatory component of the phagocytic NOX2 complex, which produces reactive oxygen species (ROS). Reactive Oxygen Species 120-143 cytochrome b-245, beta polypeptide Mus musculus 91-95 28467721-1 2017 AIMS: Neutrophil cytosolic factor 1 (NCF1) is a key regulatory component of the phagocytic NOX2 complex, which produces reactive oxygen species (ROS). Reactive Oxygen Species 145-148 cytochrome b-245, beta polypeptide Mus musculus 91-95 28467721-3 2017 In this study, we generated targeted Ncf1 knock-in mice with inducible Ncf1 expression and determined the critical time window during which the NOX2-derived ROS protect the mice from arthritis. Reactive Oxygen Species 157-160 cytochrome b-245, beta polypeptide Mus musculus 144-148 28433943-11 2017 The present study suggests that ALI-induced upregulation of neutrophilic NOX-2/ROS may contribute to depression-like symptoms in mice. Reactive Oxygen Species 79-82 cytochrome b-245, beta polypeptide Mus musculus 73-78 28760732-0 2017 Role of NOX2-Derived Reactive Oxygen Species in NK Cell-Mediated Control of Murine Melanoma Metastasis. Reactive Oxygen Species 21-44 cytochrome b-245, beta polypeptide Mus musculus 8-12 28760732-1 2017 The NADPH oxidase of myeloid cells, NOX2, generates reactive oxygen species (ROS) to eliminate pathogens and malignant cells. Reactive Oxygen Species 52-75 cytochrome b-245, beta polypeptide Mus musculus 36-40 28760732-1 2017 The NADPH oxidase of myeloid cells, NOX2, generates reactive oxygen species (ROS) to eliminate pathogens and malignant cells. Reactive Oxygen Species 77-80 cytochrome b-245, beta polypeptide Mus musculus 36-40 28760732-2 2017 NOX2-derived ROS have also been proposed to dampen functions of natural killer (NK) cells and other antineoplastic lymphocytes in the microenvironment of established tumors. Reactive Oxygen Species 13-16 cytochrome b-245, beta polypeptide Mus musculus 0-4 28760732-8 2017 We propose that NOX2-derived ROS facilitate metastasis of melanoma cells by downmodulating NK-cell function and that inhibition of NOX2 may restore IFNgamma-dependent, NK cell-mediated clearance of melanoma cells. Reactive Oxygen Species 29-32 cytochrome b-245, beta polypeptide Mus musculus 16-20 28687315-10 2017 In summary, our data suggest that the Nox2-dependent reactive oxygen species (ROS) generation contributes to the STZ-induced AD-like state. Reactive Oxygen Species 53-76 cytochrome b-245, beta polypeptide Mus musculus 38-42 28687315-10 2017 In summary, our data suggest that the Nox2-dependent reactive oxygen species (ROS) generation contributes to the STZ-induced AD-like state. Reactive Oxygen Species 78-81 cytochrome b-245, beta polypeptide Mus musculus 38-42 28804558-0 2017 NADPH oxidase 2 inhibitor diphenyleneiodonium enhances ROS-independent bacterial phagocytosis in murine macrophages via activation of the calcium-mediated p38 MAPK signaling pathway. Reactive Oxygen Species 55-58 cytochrome b-245, beta polypeptide Mus musculus 0-15 28804558-1 2017 Activation of NADPH oxidase 2 (NOX2) triggers reactive oxygen species (ROS) generation, both of which are essential for robust microbial clearance by phagocytes. Reactive Oxygen Species 46-69 cytochrome b-245, beta polypeptide Mus musculus 14-29 28804558-1 2017 Activation of NADPH oxidase 2 (NOX2) triggers reactive oxygen species (ROS) generation, both of which are essential for robust microbial clearance by phagocytes. Reactive Oxygen Species 46-69 cytochrome b-245, beta polypeptide Mus musculus 31-35 28804558-1 2017 Activation of NADPH oxidase 2 (NOX2) triggers reactive oxygen species (ROS) generation, both of which are essential for robust microbial clearance by phagocytes. Reactive Oxygen Species 71-74 cytochrome b-245, beta polypeptide Mus musculus 14-29 28804558-1 2017 Activation of NADPH oxidase 2 (NOX2) triggers reactive oxygen species (ROS) generation, both of which are essential for robust microbial clearance by phagocytes. Reactive Oxygen Species 71-74 cytochrome b-245, beta polypeptide Mus musculus 31-35 28668597-2 2017 Although it has been reported that myocardial stretch increases cellular ROS production by activating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), referred to as X-ROS signalling, the involvement of mitochondria in X-ROS is not clear. Reactive Oxygen Species 73-76 cytochrome b-245, beta polypeptide Mus musculus 102-163 28668597-2 2017 Although it has been reported that myocardial stretch increases cellular ROS production by activating nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), referred to as X-ROS signalling, the involvement of mitochondria in X-ROS is not clear. Reactive Oxygen Species 73-76 cytochrome b-245, beta polypeptide Mus musculus 165-169 27488058-6 2017 We observed that Nox2-derived reactive oxygen species via inhibition of phosphatase and tensin homolog and activation of the phosphoinositide-3-kinase (PI3K)/Akt pathway lead to activation of actin-binding protein cofilin, membrane ruffling, and macropinocytosis. Reactive Oxygen Species 30-53 cytochrome b-245, beta polypeptide Mus musculus 17-21 28433943-4 2017 NADPH oxidase (NOX-2) derived reactive oxygen species (ROS) are associated with neuropsychiatric disorders including depression. Reactive Oxygen Species 30-53 cytochrome b-245, beta polypeptide Mus musculus 15-20 28433943-4 2017 NADPH oxidase (NOX-2) derived reactive oxygen species (ROS) are associated with neuropsychiatric disorders including depression. Reactive Oxygen Species 55-58 cytochrome b-245, beta polypeptide Mus musculus 15-20 28433943-5 2017 ROS generation via NOX-2 is also shown to be involved in the pathogenesis of ALI. Reactive Oxygen Species 0-3 cytochrome b-245, beta polypeptide Mus musculus 19-24 28070636-2 2017 We previously reported that reactive oxygen species (ROS) generated by the NADPH oxidase (NOX) isoform NOX-2 are involved in chondrocyte death induced by interleukin-1beta (IL-1beta). Reactive Oxygen Species 28-51 cytochrome b-245, beta polypeptide Mus musculus 103-108 28494015-12 2017 These findings provide the first evidence that lncRNA Lethe is involved in the regulation of ROS production in macrophages through modulation of NOX2 gene expression via NFkappaB signaling. Reactive Oxygen Species 93-96 cytochrome b-245, beta polypeptide Mus musculus 145-149 28320851-0 2017 TMEM16A Contributes to Endothelial Dysfunction by Facilitating Nox2 NADPH Oxidase-Derived Reactive Oxygen Species Generation in Hypertension. Reactive Oxygen Species 90-113 cytochrome b-245, beta polypeptide Mus musculus 63-67 28320851-10 2017 Therefore, TMEM16A is a positive regulator of endothelial reactive oxygen species generation via Nox2-containing NADPH oxidase, which induces endothelial dysfunction and hypertension. Reactive Oxygen Species 58-81 cytochrome b-245, beta polypeptide Mus musculus 97-101 28070636-2 2017 We previously reported that reactive oxygen species (ROS) generated by the NADPH oxidase (NOX) isoform NOX-2 are involved in chondrocyte death induced by interleukin-1beta (IL-1beta). Reactive Oxygen Species 53-56 cytochrome b-245, beta polypeptide Mus musculus 103-108 28088753-3 2017 METHODS AND RESULTS: We have recently generated binary (Tet-ON/OFF) conditional transgenic mice (Tet-Nox2:VE-Cad-tTA) that can induce 1.8 +- 0.42-fold increase in NADPH oxidase (NOX)-derived ROS specifically in vascular endothelium upon withdrawal of tetracycline from the drinking water. Reactive Oxygen Species 191-194 cytochrome b-245, beta polypeptide Mus musculus 101-105 28301257-8 2017 These results suggest that ROS derived from gp91phox activity altered the inflammatory system and produced IL-18, which subsequently increased the expression of MUC1, thereby modulating fetal development. Reactive Oxygen Species 27-30 cytochrome b-245, beta polypeptide Mus musculus 44-52 28340575-1 2017 BACKGROUND: NADPH oxidase (NOX2) is an enzyme system that generates reactive oxygen species (ROS) in microglia and macrophages. Reactive Oxygen Species 68-91 cytochrome b-245, beta polypeptide Mus musculus 27-31 28340575-1 2017 BACKGROUND: NADPH oxidase (NOX2) is an enzyme system that generates reactive oxygen species (ROS) in microglia and macrophages. Reactive Oxygen Species 93-96 cytochrome b-245, beta polypeptide Mus musculus 27-31 28124622-12 2017 Moreover, these connexin changes are likely generated in response to reactive oxygen species generated by NOX2. Reactive Oxygen Species 69-92 cytochrome b-245, beta polypeptide Mus musculus 106-110 28951767-8 2017 Baicalin inhibited ethanol-induced expression of reactive oxygen species (ROS) generating enzymes NOX2, p67phox, xanthine oxidase, and iNOS in addition to CYP2E1 activities. Reactive Oxygen Species 49-72 cytochrome b-245, beta polypeptide Mus musculus 98-102 27607191-7 2017 In addition, there was an increase in granuloma number and size after instillation with P. acnes in mice deficient in CybB, a critical component of nicotinamide adenine dinucleotide phosphate oxidase required for the production of reactive oxygen species in the phagosome. Reactive Oxygen Species 231-254 cytochrome b-245, beta polypeptide Mus musculus 118-122 27814595-3 2017 Particulate beta-glucan has been specifically shown to engage dectin-1 receptor, which leads to the recruitment and activation of nicotinamide adenine dinucleotide phosphate oxidase-2 (NOX-2) and release of antimicrobial reactive oxygen species (ROS). Reactive Oxygen Species 221-244 cytochrome b-245, beta polypeptide Mus musculus 185-190 27814595-3 2017 Particulate beta-glucan has been specifically shown to engage dectin-1 receptor, which leads to the recruitment and activation of nicotinamide adenine dinucleotide phosphate oxidase-2 (NOX-2) and release of antimicrobial reactive oxygen species (ROS). Reactive Oxygen Species 246-249 cytochrome b-245, beta polypeptide Mus musculus 185-190 28458776-0 2017 Role of Protein Kinase C and Nox2-Derived Reactive Oxygen Species Formation in the Activation and Maturation of Dendritic Cells by Phorbol Ester and Lipopolysaccharide. Reactive Oxygen Species 42-65 cytochrome b-245, beta polypeptide Mus musculus 29-33 28458776-10 2017 Obviously Nox2-dependent ROS formation in BM-DCs is not always required for their maturation or T cell stimulatory potential. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 10-14 28831294-7 2017 Cisplatin induced the reactive oxygen species-generating enzyme NOX-2 and impaired antioxidant defense enzyme activities such as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities. Reactive Oxygen Species 22-45 cytochrome b-245, beta polypeptide Mus musculus 64-69 28951767-8 2017 Baicalin inhibited ethanol-induced expression of reactive oxygen species (ROS) generating enzymes NOX2, p67phox, xanthine oxidase, and iNOS in addition to CYP2E1 activities. Reactive Oxygen Species 74-77 cytochrome b-245, beta polypeptide Mus musculus 98-102 27231144-9 2016 Innovation and Conclusion: This is, to our knowledge, the first study addressing the development of autoimmunity in an organism with selectively compromised NOX2-dependent intracellular ROS levels. Reactive Oxygen Species 186-189 cytochrome b-245, beta polypeptide Mus musculus 157-161 27231144-2 2016 Deficiency in neutrophil cytosolic factor 1 (NCF1) inactivates the NOX2 complex, leading to a dramatic reduction of intra- and extracellular reactive oxygen species (ROS) and enhanced susceptibility to autoimmune disease. Reactive Oxygen Species 141-164 cytochrome b-245, beta polypeptide Mus musculus 67-71 27231144-2 2016 Deficiency in neutrophil cytosolic factor 1 (NCF1) inactivates the NOX2 complex, leading to a dramatic reduction of intra- and extracellular reactive oxygen species (ROS) and enhanced susceptibility to autoimmune disease. Reactive Oxygen Species 166-169 cytochrome b-245, beta polypeptide Mus musculus 67-71 27543123-9 2016 Use of a selective NOX2 inhibitor prevented increased cytosolic and nuclear/mitochondrial ROS levels and release of IL-1beta. Reactive Oxygen Species 90-93 cytochrome b-245, beta polypeptide Mus musculus 19-23 27231144-4 2016 Another component of the NOX2 complex, NCF4, directs the NOX2 complex to phagosomal membranes via binding to phosphatidylinositol 3-phosphate (PtdIns3P) and has been proposed to regulate intracellular ROS levels. Reactive Oxygen Species 201-204 cytochrome b-245, beta polypeptide Mus musculus 25-29 27231144-4 2016 Another component of the NOX2 complex, NCF4, directs the NOX2 complex to phagosomal membranes via binding to phosphatidylinositol 3-phosphate (PtdIns3P) and has been proposed to regulate intracellular ROS levels. Reactive Oxygen Species 201-204 cytochrome b-245, beta polypeptide Mus musculus 57-61 27601184-2 2016 However, the potential direct interaction between nNOS-derived nitric oxide (NO) and Nox2-derived reactive oxygen species (ROS) is poorly understood, particularly with respect to the potentiation of N-methyl-D-aspartate (NMDA) receptor activity in the spinal cord associated with the development of central sensitization. Reactive Oxygen Species 98-121 cytochrome b-245, beta polypeptide Mus musculus 85-89 27601184-2 2016 However, the potential direct interaction between nNOS-derived nitric oxide (NO) and Nox2-derived reactive oxygen species (ROS) is poorly understood, particularly with respect to the potentiation of N-methyl-D-aspartate (NMDA) receptor activity in the spinal cord associated with the development of central sensitization. Reactive Oxygen Species 123-126 cytochrome b-245, beta polypeptide Mus musculus 85-89 27601184-3 2016 Thus, the main purpose of this study was to investigate whether Sig-1R-induced and nNOS-derived NO modulates spinal Nox2 activation leading to an increase in ROS production and ultimately to the potentiation of NMDA receptor activity and pain hypersensitivity. Reactive Oxygen Species 158-161 cytochrome b-245, beta polypeptide Mus musculus 116-120 27601184-8 2016 These findings demonstrate that spinal Sig-1R-induced pain hypersensitivity is mediated by nNOS activation, which leads to an increase in Nox2 activity ultimately resulting in a ROS-induced increase in PKC-dependent pGluN1 expression. Reactive Oxygen Species 178-181 cytochrome b-245, beta polypeptide Mus musculus 138-142 27797149-2 2016 Here, we evaluated the role of the ROS produced by NADPH oxidase 2 (Nox2) and NADPH oxidase 4 (Nox4) in the self-renewal and stemness of murine induced-pluripotent stem cells (miPSCs). Reactive Oxygen Species 35-38 cytochrome b-245, beta polypeptide Mus musculus 51-66 27797149-2 2016 Here, we evaluated the role of the ROS produced by NADPH oxidase 2 (Nox2) and NADPH oxidase 4 (Nox4) in the self-renewal and stemness of murine induced-pluripotent stem cells (miPSCs). Reactive Oxygen Species 35-38 cytochrome b-245, beta polypeptide Mus musculus 68-72 27797149-3 2016 Targeted silencing of Nox2 or Nox4 reduced both NADPH oxidase activity and intracellular ROS levels, as well as alkaline phosphatase activity, the total number of miPSCs, the expression of insulin-like growth factor-1 (IGF-1), IGF-1 receptor, and the phosphorylation of extracellular signal regulated kinase (ERK) 1/2. Reactive Oxygen Species 89-92 cytochrome b-245, beta polypeptide Mus musculus 22-26 27797149-6 2016 Collectively, these results suggest that Nox2- and Nox4-derived ROS contribute to stem cell pluripotency maintenance and self-renewal. Reactive Oxygen Species 64-67 cytochrome b-245, beta polypeptide Mus musculus 41-45 27841763-7 2016 This effect was mediated by an increase in blood-brain barrier permeability that allowed angiotensin II to enter the perivascular space and activate angiotensin type 1 receptors in PVMs, leading to production of ROS through the superoxide-producing enzyme NOX2. Reactive Oxygen Species 212-215 cytochrome b-245, beta polypeptide Mus musculus 256-260 27833156-7 2016 Expression of TRPC3 C-terminal polypeptide abolished TRPC3-regulated ROS production by disrupting TRPC3-Nox2 interaction, without affecting TRPC3-mediated Ca2+ influx. Reactive Oxygen Species 69-72 cytochrome b-245, beta polypeptide Mus musculus 104-108 27990145-6 2016 Mechanistically, NOX2-dependent reactive oxygen species (ROS) production and formation of neutrophil extracellular traps were essential for the resolution of necrosis-induced inflammation: hence, by evaluating the fate of the particles at the site of inflammation, we observed that Ncf1** mice deficient in NADPH-dependent ROS failed to generate granulation tissue therefore being unable to trap the nanodiamonds. Reactive Oxygen Species 32-55 cytochrome b-245, beta polypeptide Mus musculus 17-21 27990145-6 2016 Mechanistically, NOX2-dependent reactive oxygen species (ROS) production and formation of neutrophil extracellular traps were essential for the resolution of necrosis-induced inflammation: hence, by evaluating the fate of the particles at the site of inflammation, we observed that Ncf1** mice deficient in NADPH-dependent ROS failed to generate granulation tissue therefore being unable to trap the nanodiamonds. Reactive Oxygen Species 57-60 cytochrome b-245, beta polypeptide Mus musculus 17-21 27990145-6 2016 Mechanistically, NOX2-dependent reactive oxygen species (ROS) production and formation of neutrophil extracellular traps were essential for the resolution of necrosis-induced inflammation: hence, by evaluating the fate of the particles at the site of inflammation, we observed that Ncf1** mice deficient in NADPH-dependent ROS failed to generate granulation tissue therefore being unable to trap the nanodiamonds. Reactive Oxygen Species 323-326 cytochrome b-245, beta polypeptide Mus musculus 17-21 27833156-1 2016 Reactive oxygen species (ROS) produced by NADPH oxidase 2 (Nox2) function as key mediators of mechanotransduction during both physiological adaptation to mechanical load and maladaptive remodeling of the heart. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 42-57 27477920-4 2016 NADPH oxidase (NOX2) is a critical enzyme system that generates reactive oxygen species in microglia/macrophages. Reactive Oxygen Species 64-87 cytochrome b-245, beta polypeptide Mus musculus 15-19 27833156-1 2016 Reactive oxygen species (ROS) produced by NADPH oxidase 2 (Nox2) function as key mediators of mechanotransduction during both physiological adaptation to mechanical load and maladaptive remodeling of the heart. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 59-63 27833156-1 2016 Reactive oxygen species (ROS) produced by NADPH oxidase 2 (Nox2) function as key mediators of mechanotransduction during both physiological adaptation to mechanical load and maladaptive remodeling of the heart. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 42-57 27833156-1 2016 Reactive oxygen species (ROS) produced by NADPH oxidase 2 (Nox2) function as key mediators of mechanotransduction during both physiological adaptation to mechanical load and maladaptive remodeling of the heart. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 59-63 27642005-2 2016 Here, we determine the role of ROS produced by NADPH oxidase 2 (Nox2) in the endothelial-lineage specification of mouse induced-pluripotent stem cells (miPSCs). Reactive Oxygen Species 31-34 cytochrome b-245, beta polypeptide Mus musculus 47-62 27790135-11 2016 Our study suggests that Nox2-derived reactive oxygen species (ROS) production triggers, at least in part, anesthesia- and surgery-induced hippocampal PV interneuron phenotype loss and consequent cognitive impairment in aging mice. Reactive Oxygen Species 37-60 cytochrome b-245, beta polypeptide Mus musculus 24-28 27790135-11 2016 Our study suggests that Nox2-derived reactive oxygen species (ROS) production triggers, at least in part, anesthesia- and surgery-induced hippocampal PV interneuron phenotype loss and consequent cognitive impairment in aging mice. Reactive Oxygen Species 62-65 cytochrome b-245, beta polypeptide Mus musculus 24-28 27555555-0 2016 Eliminating Nox2 reactive oxygen species production protects dystrophic skeletal muscle from pathological calcium influx assessed in vivo by manganese-enhanced magnetic resonance imaging. Reactive Oxygen Species 17-40 cytochrome b-245, beta polypeptide Mus musculus 12-16 27555555-1 2016 KEY POINTS: Inhibiting Nox2 reactive oxygen species (ROS) production reduced in vivo calcium influx in dystrophic muscle. Reactive Oxygen Species 28-51 cytochrome b-245, beta polypeptide Mus musculus 23-27 27555555-1 2016 KEY POINTS: Inhibiting Nox2 reactive oxygen species (ROS) production reduced in vivo calcium influx in dystrophic muscle. Reactive Oxygen Species 53-56 cytochrome b-245, beta polypeptide Mus musculus 23-27 27555555-2 2016 The lack of Nox2 ROS production protected against decreased in vivo muscle function in dystrophic mice. Reactive Oxygen Species 17-20 cytochrome b-245, beta polypeptide Mus musculus 12-16 27555555-7 2016 Increased Nox2 reactive oxygen species (ROS) production and sarcolemmal Ca2+ influx are early indicators of disease pathology, and eliminating Nox2 ROS production reduces aberrant Ca2+ influx in young mdx mice, a model of DMD. Reactive Oxygen Species 15-38 cytochrome b-245, beta polypeptide Mus musculus 10-14 27555555-7 2016 Increased Nox2 reactive oxygen species (ROS) production and sarcolemmal Ca2+ influx are early indicators of disease pathology, and eliminating Nox2 ROS production reduces aberrant Ca2+ influx in young mdx mice, a model of DMD. Reactive Oxygen Species 40-43 cytochrome b-245, beta polypeptide Mus musculus 10-14 27555555-7 2016 Increased Nox2 reactive oxygen species (ROS) production and sarcolemmal Ca2+ influx are early indicators of disease pathology, and eliminating Nox2 ROS production reduces aberrant Ca2+ influx in young mdx mice, a model of DMD. Reactive Oxygen Species 148-151 cytochrome b-245, beta polypeptide Mus musculus 143-147 27555555-10 2016 Therefore, we hypothesized that eliminating Nox2 ROS production would decrease calcium influx in adult mdx mice and that MEMRI would be able to monitor and differentiate disease status in dystrophic muscle. Reactive Oxygen Species 49-52 cytochrome b-245, beta polypeptide Mus musculus 44-48 27555555-11 2016 Both in vitro and in vivo data demonstrate that eliminating Nox2 ROS protected against aberrant Ca2+ influx and improved muscle function in dystrophic muscle. Reactive Oxygen Species 65-68 cytochrome b-245, beta polypeptide Mus musculus 60-64 27596335-6 2016 Notably, NOX2 increased in 14 MO ROS-producing macrophages suggesting that macrophages and NOX contribute to SCI oxidative stress. Reactive Oxygen Species 33-36 cytochrome b-245, beta polypeptide Mus musculus 9-13 27642005-2 2016 Here, we determine the role of ROS produced by NADPH oxidase 2 (Nox2) in the endothelial-lineage specification of mouse induced-pluripotent stem cells (miPSCs). Reactive Oxygen Species 31-34 cytochrome b-245, beta polypeptide Mus musculus 64-68 27642005-4 2016 Higher levels of Nox2 expression increased Notch signaling and arterial EC differentiation, and this increase was abolished by the inhibition of ROS generation or by the silencing of Notch1 expression. Reactive Oxygen Species 145-148 cytochrome b-245, beta polypeptide Mus musculus 17-21 27642005-6 2016 Taken together, these observations indicate that Nox2-mediated ROS production promotes arterial EC specification in differentiating miPSCs by activating the Notch signaling pathway and contributes to the angiogenic potency of transplanted miPSC-derived ECs. Reactive Oxygen Species 63-66 cytochrome b-245, beta polypeptide Mus musculus 49-53 27397876-2 2016 NADPH oxidase-2 (Nox2) is a major ROS source within the heart and its activity increases after MI. Reactive Oxygen Species 34-37 cytochrome b-245, beta polypeptide Mus musculus 0-15 27427418-3 2016 We investigated mannan-induced arthritis in SKG mice and how NADPH oxidase 2-derived reactive oxygen species (ROS) regulate disease. Reactive Oxygen Species 85-108 cytochrome b-245, beta polypeptide Mus musculus 61-76 27427418-3 2016 We investigated mannan-induced arthritis in SKG mice and how NADPH oxidase 2-derived reactive oxygen species (ROS) regulate disease. Reactive Oxygen Species 110-113 cytochrome b-245, beta polypeptide Mus musculus 61-76 27397876-2 2016 NADPH oxidase-2 (Nox2) is a major ROS source within the heart and its activity increases after MI. Reactive Oxygen Species 34-37 cytochrome b-245, beta polypeptide Mus musculus 17-21 26988594-6 2016 Consistently, production of ROS was inhibited in NOX1(-/Y) platelets stimulated with thrombin, but not collagen-related peptide, whereas NOX2(-/-) platelets showed reduced ROS generation induced by collagen-related peptide or thrombin. Reactive Oxygen Species 172-175 cytochrome b-245, beta polypeptide Mus musculus 137-141 27107694-8 2016 Geraniol therefore protects against endothelial dysfunction induced by HFD through reducing NOX-2 associated ROS generation. Reactive Oxygen Species 109-112 cytochrome b-245, beta polypeptide Mus musculus 92-97 27266634-7 2016 Further, use of a specific NADPH oxidase-2 inhibitor to limit ROS production prevents neointima formation in Nf1(+/-) mice. Reactive Oxygen Species 62-65 cytochrome b-245, beta polypeptide Mus musculus 27-42 27044504-2 2016 Nox2), p47(phox), p67(phox), p22(phox), p40(phox)) leading to reduced phagocyte-derived reactive oxygen species production. Reactive Oxygen Species 88-111 cytochrome b-245, beta polypeptide Mus musculus 0-4 27003327-10 2016 We found that ROS which responsible for myofibroblasts activation was mainly from AMs and was NOX2 and NOX4 dependent. Reactive Oxygen Species 14-17 cytochrome b-245, beta polypeptide Mus musculus 94-98 26895661-7 2016 Cellular accumulation of reactive oxygen species was significantly reduced by ASTX, which was attributable to a decrease in NADPH oxidase 2 expression. Reactive Oxygen Species 25-48 cytochrome b-245, beta polypeptide Mus musculus 124-139 27033790-9 2016 Activation of ALDH2 could exert cytoprotection via inhibiting NOX2-dependent ROS production. Reactive Oxygen Species 77-80 cytochrome b-245, beta polypeptide Mus musculus 62-66 26852953-6 2016 In addition, HTMC inhibited reactive oxygen species (ROS) production by reducing NADPH oxidase (Nox) 2 and Nox4 expression. Reactive Oxygen Species 28-51 cytochrome b-245, beta polypeptide Mus musculus 81-102 26852953-6 2016 In addition, HTMC inhibited reactive oxygen species (ROS) production by reducing NADPH oxidase (Nox) 2 and Nox4 expression. Reactive Oxygen Species 53-56 cytochrome b-245, beta polypeptide Mus musculus 81-102 26756466-8 2016 Inhibitors of PKC or NOX2 prevent mitochondrial dysfunction and the increase in ROS, demonstrating that PKC-NOX2 activation is also required for amplification of palmitate induced-ROS. Reactive Oxygen Species 80-83 cytochrome b-245, beta polypeptide Mus musculus 21-25 26756466-8 2016 Inhibitors of PKC or NOX2 prevent mitochondrial dysfunction and the increase in ROS, demonstrating that PKC-NOX2 activation is also required for amplification of palmitate induced-ROS. Reactive Oxygen Species 80-83 cytochrome b-245, beta polypeptide Mus musculus 108-112 26756466-8 2016 Inhibitors of PKC or NOX2 prevent mitochondrial dysfunction and the increase in ROS, demonstrating that PKC-NOX2 activation is also required for amplification of palmitate induced-ROS. Reactive Oxygen Species 180-183 cytochrome b-245, beta polypeptide Mus musculus 108-112 26756466-10 2016 We conclude that palmitate induces mitochondrial ROS that is amplified by NOX2, causing greater mitochondrial ROS generation and partial depolarization of the mitochondrial inner membrane. Reactive Oxygen Species 49-52 cytochrome b-245, beta polypeptide Mus musculus 74-78 26756466-10 2016 We conclude that palmitate induces mitochondrial ROS that is amplified by NOX2, causing greater mitochondrial ROS generation and partial depolarization of the mitochondrial inner membrane. Reactive Oxygen Species 110-113 cytochrome b-245, beta polypeptide Mus musculus 74-78 26890413-4 2016 Recent evidence demonstrates that enhanced reactive oxygen species (ROS) production by CYBB/NOX2 impairs autophagy in muscles from the dmd/mdx mouse, a genetic model of Duchenne muscular dystrophy. Reactive Oxygen Species 43-66 cytochrome b-245, beta polypeptide Mus musculus 87-91 26890413-4 2016 Recent evidence demonstrates that enhanced reactive oxygen species (ROS) production by CYBB/NOX2 impairs autophagy in muscles from the dmd/mdx mouse, a genetic model of Duchenne muscular dystrophy. Reactive Oxygen Species 43-66 cytochrome b-245, beta polypeptide Mus musculus 92-96 26890413-4 2016 Recent evidence demonstrates that enhanced reactive oxygen species (ROS) production by CYBB/NOX2 impairs autophagy in muscles from the dmd/mdx mouse, a genetic model of Duchenne muscular dystrophy. Reactive Oxygen Species 68-71 cytochrome b-245, beta polypeptide Mus musculus 87-91 26890413-4 2016 Recent evidence demonstrates that enhanced reactive oxygen species (ROS) production by CYBB/NOX2 impairs autophagy in muscles from the dmd/mdx mouse, a genetic model of Duchenne muscular dystrophy. Reactive Oxygen Species 68-71 cytochrome b-245, beta polypeptide Mus musculus 92-96 26648475-0 2016 Gp91phox-derived Reactive Oxygen Species/Urocortin 2/Corticotropin-releasing Hormone Receptor Type 2 Play an Important Role in Long-term Ultraviolet A Eye Irradiation-induced Photoaging. Reactive Oxygen Species 17-40 cytochrome b-245, beta polypeptide Mus musculus 0-8 26254234-0 2016 NADPH oxidase 2-derived reactive oxygen species in the hippocampus might contribute to microglial activation in postoperative cognitive dysfunction in aged mice. Reactive Oxygen Species 24-47 cytochrome b-245, beta polypeptide Mus musculus 0-15 26254234-2 2016 Nox2, one of the main isoforms of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in the central nervous system, is a predominant source of reactive oxygen species (ROS) overproduction in phagocytes including microglia. Reactive Oxygen Species 152-175 cytochrome b-245, beta polypeptide Mus musculus 0-4 26254234-2 2016 Nox2, one of the main isoforms of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in the central nervous system, is a predominant source of reactive oxygen species (ROS) overproduction in phagocytes including microglia. Reactive Oxygen Species 177-180 cytochrome b-245, beta polypeptide Mus musculus 0-4 26254234-11 2016 Together, our data suggested that Nox2-derived ROS in hippocampal microglia, at least in part, contributes to subsequent neuroinflammation and cognitive impairments induced by surgery in aged mice. Reactive Oxygen Species 47-50 cytochrome b-245, beta polypeptide Mus musculus 34-38 27467102-3 2016 Recent evidence suggests that excessive generation of reactive oxygen species (ROS) by the phagocyte-like NADPH oxidase2 (Nox2), along with significantly low levels of antioxidants in beta-cells, drive them toward oxidative damage. Reactive Oxygen Species 54-77 cytochrome b-245, beta polypeptide Mus musculus 106-120 27467102-3 2016 Recent evidence suggests that excessive generation of reactive oxygen species (ROS) by the phagocyte-like NADPH oxidase2 (Nox2), along with significantly low levels of antioxidants in beta-cells, drive them toward oxidative damage. Reactive Oxygen Species 54-77 cytochrome b-245, beta polypeptide Mus musculus 122-126 27467102-3 2016 Recent evidence suggests that excessive generation of reactive oxygen species (ROS) by the phagocyte-like NADPH oxidase2 (Nox2), along with significantly low levels of antioxidants in beta-cells, drive them toward oxidative damage. Reactive Oxygen Species 79-82 cytochrome b-245, beta polypeptide Mus musculus 106-120 27467102-3 2016 Recent evidence suggests that excessive generation of reactive oxygen species (ROS) by the phagocyte-like NADPH oxidase2 (Nox2), along with significantly low levels of antioxidants in beta-cells, drive them toward oxidative damage. Reactive Oxygen Species 79-82 cytochrome b-245, beta polypeptide Mus musculus 122-126 26552047-10 2016 Furthermore, NOX2TG-Akita mice exhibited distinct phenotypic changes in glomerular mesangial cells expressing alpha-smooth muscle actin, and in podocytes expressing increased levels of desmin, whereas the glomeruli generated increased levels of ROS. Reactive Oxygen Species 245-248 cytochrome b-245, beta polypeptide Mus musculus 13-19 26648475-9 2016 These results indicate that long-term UVA eye irradiation led to increased gp91phox-derived ROS in the brain and the increased expression of urocortin 2 and CRHR type 2, resulting in photoaging; however, further studies are needed to confirm these findings. Reactive Oxygen Species 92-95 cytochrome b-245, beta polypeptide Mus musculus 75-83 26054376-2 2015 We and others demonstrated that NOX1/2 NADPH oxidase inhibition, by genetic deletion of p47phox, in Apoe(-/-) mice decreases vascular reactive oxygen species (ROS) generation and atherosclerosis in young age. Reactive Oxygen Species 134-157 cytochrome b-245, beta polypeptide Mus musculus 32-38 26054376-2 2015 We and others demonstrated that NOX1/2 NADPH oxidase inhibition, by genetic deletion of p47phox, in Apoe(-/-) mice decreases vascular reactive oxygen species (ROS) generation and atherosclerosis in young age. Reactive Oxygen Species 159-162 cytochrome b-245, beta polypeptide Mus musculus 32-38 26503985-12 2015 CONCLUSIONS: Our studies suggest that downregulation of miR-448-3p leads to the increase in the expression of Ncf1 gene and p47(phox) protein, as well as to the substantial increase in NOX2-derived ROS production. Reactive Oxygen Species 198-201 cytochrome b-245, beta polypeptide Mus musculus 185-189 26135714-8 2015 Following systemic administration in mice, GSK2795039 abolished the production of ROS by activated NOX2 enzyme in a paw inflammation model. Reactive Oxygen Species 82-85 cytochrome b-245, beta polypeptide Mus musculus 99-103 26333777-4 2015 Platelet NOX2-produced reactive oxygen species (ROS) regulated P-selectin exposure upon agonist stimulation and the ligand-binding function of glycoprotein Ibalpha. Reactive Oxygen Species 23-46 cytochrome b-245, beta polypeptide Mus musculus 9-13 26333777-4 2015 Platelet NOX2-produced reactive oxygen species (ROS) regulated P-selectin exposure upon agonist stimulation and the ligand-binding function of glycoprotein Ibalpha. Reactive Oxygen Species 48-51 cytochrome b-245, beta polypeptide Mus musculus 9-13 26333777-5 2015 Furthermore, neutrophil NOX2-generated ROS enhanced the activation and ligand-binding activity of alphaMbeta2 integrin following N-formyl-methionyl-leucyl phenylalanine stimulation. Reactive Oxygen Species 39-42 cytochrome b-245, beta polypeptide Mus musculus 24-28 26333777-9 2015 Our results indicate that platelet and neutrophil NOX2-produced ROS are critical for the function of surface receptors essential for neutrophil-platelet interactions during vascular inflammation. Reactive Oxygen Species 64-67 cytochrome b-245, beta polypeptide Mus musculus 50-54 26555638-7 2015 Finally, it was shown that ROS production in mdx mice is proportional to the activity of RyR2-mediated SR Ca(2+) leak, and likely generated by Nox2. Reactive Oxygen Species 27-30 cytochrome b-245, beta polypeptide Mus musculus 143-147 26184620-3 2015 Recent studies found that Nox2-mediated reactive oxygen species production modulates physiological cardiomyocyte function. Reactive Oxygen Species 40-63 cytochrome b-245, beta polypeptide Mus musculus 26-30 26076008-0 2015 Methylcholanthrene-Induced Sarcomas Develop Independently from NOX2-Derived ROS. Reactive Oxygen Species 76-79 cytochrome b-245, beta polypeptide Mus musculus 63-67 26076008-1 2015 Reactive oxygen species (ROS) produced by the inducible NADPH oxidase type 2 (NOX2) complex are essential for clearing certain infectious organisms but may also have a role in regulating inflammation and immune response. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 56-76 26076008-1 2015 Reactive oxygen species (ROS) produced by the inducible NADPH oxidase type 2 (NOX2) complex are essential for clearing certain infectious organisms but may also have a role in regulating inflammation and immune response. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 78-82 26076008-1 2015 Reactive oxygen species (ROS) produced by the inducible NADPH oxidase type 2 (NOX2) complex are essential for clearing certain infectious organisms but may also have a role in regulating inflammation and immune response. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 56-76 26076008-1 2015 Reactive oxygen species (ROS) produced by the inducible NADPH oxidase type 2 (NOX2) complex are essential for clearing certain infectious organisms but may also have a role in regulating inflammation and immune response. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 78-82 26076008-4 2015 In this study we aimed to decipher the role of NOX2-derived ROS in a chemically (by methylcholanthrene (MCA)) induced sarcoma model. Reactive Oxygen Species 60-63 cytochrome b-245, beta polypeptide Mus musculus 47-51 25825489-2 2015 Although the role of Nox2, a major ROS-generating enzyme, is well described in host defense and inflammation, little is known about its potential role in insulin resistance in skeletal muscle. Reactive Oxygen Species 35-38 cytochrome b-245, beta polypeptide Mus musculus 21-25 25922068-0 2015 p47phox-Nox2-dependent ROS Signaling Inhibits Early Bone Development in Mice but Protects against Skeletal Aging. Reactive Oxygen Species 23-26 cytochrome b-245, beta polypeptide Mus musculus 8-12 25922068-10 2015 These data indicate that the observed age-related switch of bone mass in p47(phox)-deficient mice occurs through an increased inflammatory milieu in bone and that p47(phox)-Nox2-dependent physiological ROS signaling suppresses inflammation in aging. Reactive Oxygen Species 202-205 cytochrome b-245, beta polypeptide Mus musculus 173-177 25825489-8 2015 These data indicate that increased production of ROS in insulin resistance induced by high glucose in skeletal muscle cells is a consequence of Nox2 activation. Reactive Oxygen Species 49-52 cytochrome b-245, beta polypeptide Mus musculus 144-148 25689796-1 2015 The NADPH oxidase 2 (NOX2) complex is responsible for the production of ROS in phagocytic cells. Reactive Oxygen Species 72-75 cytochrome b-245, beta polypeptide Mus musculus 4-19 25760962-1 2015 The phagocyte NADPH oxidase NOX2 produces reactive oxygen species (ROS) and is a well-known player in host defence. Reactive Oxygen Species 42-65 cytochrome b-245, beta polypeptide Mus musculus 28-32 25760962-1 2015 The phagocyte NADPH oxidase NOX2 produces reactive oxygen species (ROS) and is a well-known player in host defence. Reactive Oxygen Species 67-70 cytochrome b-245, beta polypeptide Mus musculus 28-32 25760962-9 2015 NOX2-dependent ROS generation is well documented for dendritic cells and B-lymphocytes. Reactive Oxygen Species 15-18 cytochrome b-245, beta polypeptide Mus musculus 0-4 25760962-14 2015 In dendritic cells, NOX2-derived ROS might be important for antigen processing and cell activation. Reactive Oxygen Species 33-36 cytochrome b-245, beta polypeptide Mus musculus 20-24 25689796-1 2015 The NADPH oxidase 2 (NOX2) complex is responsible for the production of ROS in phagocytic cells. Reactive Oxygen Species 72-75 cytochrome b-245, beta polypeptide Mus musculus 21-25 25116588-11 2015 Compared to WT mice, the lack of functional NOX2 led to decreased elastase-induced ROS production and protected against emphysema. Reactive Oxygen Species 83-86 cytochrome b-245, beta polypeptide Mus musculus 44-48 25565313-2 2015 Major ROS generators in the glomerulus of the kidney are the p47(phox)-containing NAPDH oxidases NOX1 and NOX2. Reactive Oxygen Species 6-9 cytochrome b-245, beta polypeptide Mus musculus 106-110 25892960-0 2015 NOD2 is involved in the inflammatory response after cerebral ischemia-reperfusion injury and triggers NADPH oxidase 2-derived reactive oxygen species. Reactive Oxygen Species 126-149 cytochrome b-245, beta polypeptide Mus musculus 102-117 25710879-5 2015 oxLDL-induced ROS generation was blocked by the reduced NAD phosphate oxidase 2 (NOX2) inhibitor, gp91ds-tat, and absent in NOX2(-/-) mice. Reactive Oxygen Species 14-17 cytochrome b-245, beta polypeptide Mus musculus 56-79 25710879-5 2015 oxLDL-induced ROS generation was blocked by the reduced NAD phosphate oxidase 2 (NOX2) inhibitor, gp91ds-tat, and absent in NOX2(-/-) mice. Reactive Oxygen Species 14-17 cytochrome b-245, beta polypeptide Mus musculus 81-85 25799045-1 2015 Previous studies have demonstrated that the cell surface receptor Slamf1 (CD150) is requisite for optimal NADPH-oxidase (Nox2) dependent reactive oxygen species (ROS) production by phagocytes in response to Gram- bacteria. Reactive Oxygen Species 137-160 cytochrome b-245, beta polypeptide Mus musculus 121-125 25799045-1 2015 Previous studies have demonstrated that the cell surface receptor Slamf1 (CD150) is requisite for optimal NADPH-oxidase (Nox2) dependent reactive oxygen species (ROS) production by phagocytes in response to Gram- bacteria. Reactive Oxygen Species 162-165 cytochrome b-245, beta polypeptide Mus musculus 121-125 25637741-1 2015 Lung injury associated with hyperoxia reflects in part the secondary effects of pulmonary inflammation and the associated production of reactive oxygen species due to activation of NADPH oxidase, type 2 (NOX2). Reactive Oxygen Species 136-159 cytochrome b-245, beta polypeptide Mus musculus 181-202 25637741-1 2015 Lung injury associated with hyperoxia reflects in part the secondary effects of pulmonary inflammation and the associated production of reactive oxygen species due to activation of NADPH oxidase, type 2 (NOX2). Reactive Oxygen Species 136-159 cytochrome b-245, beta polypeptide Mus musculus 204-208 25474113-5 2014 The deficiency of NOX2 mediated ROS was compensated by higher level of inducible nitric oxide synthase (iNOS) expression, and nitric oxide and inflammatory cytokine (TNF-alpha, IFN-gamma, IL-1beta) release by p47(phox-/-) macrophages as compared to that noted in WT controls infected by T. cruzi. Reactive Oxygen Species 32-35 cytochrome b-245, beta polypeptide Mus musculus 18-22 24844655-0 2014 SYNCRIP-dependent Nox2 mRNA destabilization impairs ROS formation in M2-polarized macrophages. Reactive Oxygen Species 52-55 cytochrome b-245, beta polypeptide Mus musculus 18-22 24844655-4 2014 Here, we provide mechanistic insights into diminished mRNA stability of the NADPH oxidase Nox2 on macrophage M2 polarization and therefore reduced ROS formation in sepsis. Reactive Oxygen Species 147-150 cytochrome b-245, beta polypeptide Mus musculus 90-94 25502554-11 2014 We conclude that NOX2 is a major source of ROS in prion diseases and can affect prion pathogenesis. Reactive Oxygen Species 43-46 cytochrome b-245, beta polypeptide Mus musculus 17-21 24787605-1 2014 AIMS: Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by mutations in the phagocyte reactive oxygen species (ROS)-producing NOX2 enzyme complex and characterized by recurrent infections associated with hyperinflammatory and autoimmune manifestations. Reactive Oxygen Species 134-137 cytochrome b-245, beta polypeptide Mus musculus 149-153 24787605-6 2014 INNOVATION: Our findings link the previously unexplained connection between ROS deficiency and increased susceptibility to autoimmunity by the discovery that activation of IFN signaling is a major pathway downstream of a deficient NOX2 complex in both mice and humans. Reactive Oxygen Species 76-79 cytochrome b-245, beta polypeptide Mus musculus 231-235 24787605-1 2014 AIMS: Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by mutations in the phagocyte reactive oxygen species (ROS)-producing NOX2 enzyme complex and characterized by recurrent infections associated with hyperinflammatory and autoimmune manifestations. Reactive Oxygen Species 109-132 cytochrome b-245, beta polypeptide Mus musculus 149-153 25268765-6 2014 Level of reactive oxygen species (ROS) was reduced by DDS treatment, which may due to decreased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and NOX2 expression. Reactive Oxygen Species 9-32 cytochrome b-245, beta polypeptide Mus musculus 169-173 25178511-2 2014 Increased ROS has been observed in the amyotrophic lateral sclerosis (ALS) SOD1 transgenic mouse, and in this preclinical model the inactivation of NOX2 decreases ROS production and extends survival. Reactive Oxygen Species 10-13 cytochrome b-245, beta polypeptide Mus musculus 148-152 25178511-2 2014 Increased ROS has been observed in the amyotrophic lateral sclerosis (ALS) SOD1 transgenic mouse, and in this preclinical model the inactivation of NOX2 decreases ROS production and extends survival. Reactive Oxygen Species 163-166 cytochrome b-245, beta polypeptide Mus musculus 148-152 25268765-6 2014 Level of reactive oxygen species (ROS) was reduced by DDS treatment, which may due to decreased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and NOX2 expression. Reactive Oxygen Species 34-37 cytochrome b-245, beta polypeptide Mus musculus 169-173 24850909-9 2014 Knockdown of LKB1 restored gAcrp-suppressed Nox2 expression, suggesting that LKB1/AMPK pathway plays a critical role in the suppression of ethanol-induced ROS production and activation of NADPH oxidase by gAcrp. Reactive Oxygen Species 155-158 cytochrome b-245, beta polypeptide Mus musculus 44-48 24631921-7 2014 Inhibition of NOX-2 diminished both ROS production and induction of IL-6 expression. Reactive Oxygen Species 36-39 cytochrome b-245, beta polypeptide Mus musculus 14-19 25139590-3 2014 We here detected the ROS-generating nicotinamide adenine dinucleotide phosphate oxidase isoform Nox2 in macrophages of dorsal root ganglia (DRG) in mice. Reactive Oxygen Species 21-24 cytochrome b-245, beta polypeptide Mus musculus 96-100 25139590-4 2014 In response to peripheral nerve injury, Nox2-positive macrophages were recruited to DRG, and ROS production was increased in a Nox2-dependent manner. Reactive Oxygen Species 93-96 cytochrome b-245, beta polypeptide Mus musculus 127-131 25139590-7 2014 These data suggest that Nox2-dependent ROS production in macrophages recruited to DRG contributes to neuropathic pain hypersensitivity, underlining the observation that Nox-derived ROS exert specific functions during the processing of pain. Reactive Oxygen Species 39-42 cytochrome b-245, beta polypeptide Mus musculus 24-28 25139590-7 2014 These data suggest that Nox2-dependent ROS production in macrophages recruited to DRG contributes to neuropathic pain hypersensitivity, underlining the observation that Nox-derived ROS exert specific functions during the processing of pain. Reactive Oxygen Species 181-184 cytochrome b-245, beta polypeptide Mus musculus 24-28 25188296-1 2014 Patients with chronic granulomatous disease (CGD) lack generation of reactive oxygen species (ROS) through the phagocyte NADPH oxidase NOX2. Reactive Oxygen Species 69-92 cytochrome b-245, beta polypeptide Mus musculus 135-139 25188296-1 2014 Patients with chronic granulomatous disease (CGD) lack generation of reactive oxygen species (ROS) through the phagocyte NADPH oxidase NOX2. Reactive Oxygen Species 94-97 cytochrome b-245, beta polypeptide Mus musculus 135-139 24991871-0 2014 Chronic aldosterone administration causes Nox2-mediated increases in reactive oxygen species production and endothelial dysfunction in the cerebral circulation. Reactive Oxygen Species 69-92 cytochrome b-245, beta polypeptide Mus musculus 42-46 24991871-4 2014 Because Nox2-containing NADPH oxidase (Nox2 oxidase) is highly expressed in the cerebral endothelium, we postulated that it might contribute to ROS generation and vascular dysfunction in response to aldosterone. Reactive Oxygen Species 144-147 cytochrome b-245, beta polypeptide Mus musculus 8-12 24991871-4 2014 Because Nox2-containing NADPH oxidase (Nox2 oxidase) is highly expressed in the cerebral endothelium, we postulated that it might contribute to ROS generation and vascular dysfunction in response to aldosterone. Reactive Oxygen Species 144-147 cytochrome b-245, beta polypeptide Mus musculus 39-43 24991871-5 2014 Here, we examined the effect of aldosterone and Nox2 oxidase on ROS production and endothelial dysfunction in the cerebral circulation, and whether the effects of aldosterone are exacerbated in aged mice. Reactive Oxygen Species 64-67 cytochrome b-245, beta polypeptide Mus musculus 48-52 24991871-10 2014 CONCLUSION: These data indicate that Nox2 oxidase mediates aldosterone-induced increases in ROS production and endothelial dysfunction in cerebral arteries from adult mice independently of blood pressure changes. Reactive Oxygen Species 92-95 cytochrome b-245, beta polypeptide Mus musculus 37-41 25150938-7 2014 Levels of NADPH oxidase 2-derived reactive oxygen species were approximately 9 times higher in the hypoxia group. Reactive Oxygen Species 34-57 cytochrome b-245, beta polypeptide Mus musculus 10-25 23700158-1 2014 Apocynin is known to suppress the production of reactive oxygen species (ROS) by inhibiting NADPH oxidases, specifically phagocytic NADPH oxidase (PHOX or NOX2). Reactive Oxygen Species 73-76 cytochrome b-245, beta polypeptide Mus musculus 155-159 24571599-0 2014 The role of Nox2-derived ROS in the development of cognitive impairment after sepsis. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 12-16 25028121-7 2014 Genetic downregulation of Nox2 activity in the mdx mouse decreases reactive oxygen species (ROS) production, abrogates defective autophagy and rescues histological abnormalities and contractile impairment. Reactive Oxygen Species 67-90 cytochrome b-245, beta polypeptide Mus musculus 26-30 25028121-7 2014 Genetic downregulation of Nox2 activity in the mdx mouse decreases reactive oxygen species (ROS) production, abrogates defective autophagy and rescues histological abnormalities and contractile impairment. Reactive Oxygen Species 92-95 cytochrome b-245, beta polypeptide Mus musculus 26-30 24807872-3 2014 METHODS AND RESULTS: A specific increase in endothelial ROS production in Nox2 transgenic mice was sufficient to cause Ang II-mediated aortic dissection, which was never observed in wild-type mice. Reactive Oxygen Species 56-59 cytochrome b-245, beta polypeptide Mus musculus 74-78 24807872-4 2014 Nox2 transgenic aortas had increased endothelial ROS production, endothelial vascular cell adhesion molecule-1 expression, matrix metalloproteinase activity, and CD45(+) inflammatory cell infiltration. Reactive Oxygen Species 49-52 cytochrome b-245, beta polypeptide Mus musculus 0-4 24524998-0 2014 Serotonin regulates innate immune responses of colon epithelial cells through Nox2-derived reactive oxygen species. Reactive Oxygen Species 91-114 cytochrome b-245, beta polypeptide Mus musculus 78-82 24524998-4 2014 Nox2-derived production of ROS corresponded with the rapid and brief activation of Rac. Reactive Oxygen Species 27-30 cytochrome b-245, beta polypeptide Mus musculus 0-4 24256560-11 2014 In vitro EtOH exposure of ST2 cells increased ROS, which was blocked by pretreating with DPI or the NOX2 inhibitor gliotoxin. Reactive Oxygen Species 46-49 cytochrome b-245, beta polypeptide Mus musculus 100-104 24256560-13 2014 CONCLUSIONS: These data suggest that NOX2-derived ROS is necessary for EtOH-induced bone resorption. Reactive Oxygen Species 50-53 cytochrome b-245, beta polypeptide Mus musculus 37-41 24571599-12 2014 CONCLUSIONS: Our results demonstrate that Nox2 is the main source of reactive oxygen species (ROS) involved in the oxidative damage to the hippocampus in SAE and that Nox2-derived ROS are determining factors for cognitive impairments after sepsis. Reactive Oxygen Species 69-92 cytochrome b-245, beta polypeptide Mus musculus 42-46 24571599-12 2014 CONCLUSIONS: Our results demonstrate that Nox2 is the main source of reactive oxygen species (ROS) involved in the oxidative damage to the hippocampus in SAE and that Nox2-derived ROS are determining factors for cognitive impairments after sepsis. Reactive Oxygen Species 94-97 cytochrome b-245, beta polypeptide Mus musculus 42-46 24571599-12 2014 CONCLUSIONS: Our results demonstrate that Nox2 is the main source of reactive oxygen species (ROS) involved in the oxidative damage to the hippocampus in SAE and that Nox2-derived ROS are determining factors for cognitive impairments after sepsis. Reactive Oxygen Species 180-183 cytochrome b-245, beta polypeptide Mus musculus 167-171 24571599-13 2014 These findings highlight the importance of Nox2-derived ROS as a central mechanism in the development of neuroinflammation associated with SAE. Reactive Oxygen Species 56-59 cytochrome b-245, beta polypeptide Mus musculus 43-47 24318114-5 2014 NADPH oxidase 2 (NOX2) has been reported to be a major source of ROS with pulmonary inflammation. Reactive Oxygen Species 65-68 cytochrome b-245, beta polypeptide Mus musculus 0-15 23758611-1 2014 AIMS: We reported earlier that ischemia results in the generation of reactive oxygen species (ROS) via the closure of a K(ATP) channel which causes membrane depolarization and NADPH oxidase 2 (NOX2) activation. Reactive Oxygen Species 69-92 cytochrome b-245, beta polypeptide Mus musculus 176-191 23758611-1 2014 AIMS: We reported earlier that ischemia results in the generation of reactive oxygen species (ROS) via the closure of a K(ATP) channel which causes membrane depolarization and NADPH oxidase 2 (NOX2) activation. Reactive Oxygen Species 69-92 cytochrome b-245, beta polypeptide Mus musculus 193-197 23758611-1 2014 AIMS: We reported earlier that ischemia results in the generation of reactive oxygen species (ROS) via the closure of a K(ATP) channel which causes membrane depolarization and NADPH oxidase 2 (NOX2) activation. Reactive Oxygen Species 94-97 cytochrome b-245, beta polypeptide Mus musculus 176-191 23758611-1 2014 AIMS: We reported earlier that ischemia results in the generation of reactive oxygen species (ROS) via the closure of a K(ATP) channel which causes membrane depolarization and NADPH oxidase 2 (NOX2) activation. Reactive Oxygen Species 94-97 cytochrome b-245, beta polypeptide Mus musculus 193-197 24318114-5 2014 NADPH oxidase 2 (NOX2) has been reported to be a major source of ROS with pulmonary inflammation. Reactive Oxygen Species 65-68 cytochrome b-245, beta polypeptide Mus musculus 17-21 24213612-4 2014 Here we postulate that acute pressure overload induced by pulmonary artery banding (PAB) leads to a Nox4-initiated increase in reactive oxygen species (ROS) in mouse RV that may lead to feed-forward induction of Nox2. Reactive Oxygen Species 127-150 cytochrome b-245, beta polypeptide Mus musculus 212-216 24380729-8 2014 The Pak1 dependent increase in ROS was attenuated in VMs deficient for NADPH oxidase 2 (NOX2; p47(phox-/-)) or in VMs where NOX2 was inhibited (gp91ds-tat). Reactive Oxygen Species 31-34 cytochrome b-245, beta polypeptide Mus musculus 71-86 24380729-8 2014 The Pak1 dependent increase in ROS was attenuated in VMs deficient for NADPH oxidase 2 (NOX2; p47(phox-/-)) or in VMs where NOX2 was inhibited (gp91ds-tat). Reactive Oxygen Species 31-34 cytochrome b-245, beta polypeptide Mus musculus 88-92 24380729-8 2014 The Pak1 dependent increase in ROS was attenuated in VMs deficient for NADPH oxidase 2 (NOX2; p47(phox-/-)) or in VMs where NOX2 was inhibited (gp91ds-tat). Reactive Oxygen Species 31-34 cytochrome b-245, beta polypeptide Mus musculus 124-128 24380729-9 2014 Voltage clamp recordings showed increased NCX activity in Pak1(-/-) VMs that depended on enhanced NOX2 induced ROS production. Reactive Oxygen Species 111-114 cytochrome b-245, beta polypeptide Mus musculus 98-102 24270180-1 2014 OBJECTIVES: To investigate whether NADPH oxidase 2 (NOX2), a major source of reactive oxygen species (ROS), contributes to the emergence of arterial hypertension in a murine model of sleep apnea. Reactive Oxygen Species 77-100 cytochrome b-245, beta polypeptide Mus musculus 35-50 24270180-1 2014 OBJECTIVES: To investigate whether NADPH oxidase 2 (NOX2), a major source of reactive oxygen species (ROS), contributes to the emergence of arterial hypertension in a murine model of sleep apnea. Reactive Oxygen Species 77-100 cytochrome b-245, beta polypeptide Mus musculus 52-56 24270180-1 2014 OBJECTIVES: To investigate whether NADPH oxidase 2 (NOX2), a major source of reactive oxygen species (ROS), contributes to the emergence of arterial hypertension in a murine model of sleep apnea. Reactive Oxygen Species 102-105 cytochrome b-245, beta polypeptide Mus musculus 35-50 24270180-1 2014 OBJECTIVES: To investigate whether NADPH oxidase 2 (NOX2), a major source of reactive oxygen species (ROS), contributes to the emergence of arterial hypertension in a murine model of sleep apnea. Reactive Oxygen Species 102-105 cytochrome b-245, beta polypeptide Mus musculus 52-56 24270180-9 2014 CONCLUSION: We suggest that the CIH-induced arterial hypertension is mediated by ROS derived from an activation of NOX2 within cells located outside the cardiovascular system. Reactive Oxygen Species 81-84 cytochrome b-245, beta polypeptide Mus musculus 115-119 24213612-4 2014 Here we postulate that acute pressure overload induced by pulmonary artery banding (PAB) leads to a Nox4-initiated increase in reactive oxygen species (ROS) in mouse RV that may lead to feed-forward induction of Nox2. Reactive Oxygen Species 152-155 cytochrome b-245, beta polypeptide Mus musculus 212-216 24053613-11 2014 INNOVATION AND CONCLUSIONS: These studies show that Nox2 stimulates mitochondrial ROS by activating reverse electron transfer and both mitochondrial O2( -) and reverse electron transfer may represent new pharmacological targets for the treatment of hypertension. Reactive Oxygen Species 82-85 cytochrome b-245, beta polypeptide Mus musculus 52-56 24358335-1 2013 The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. Reactive Oxygen Species 65-88 cytochrome b-245, beta polypeptide Mus musculus 4-19 24104877-6 2014 DGT-dependent ROS was suppressed by the inhibition of PI3K, PKC, and the mitochondrial KATP channel, suggesting roles for these proteins, respectively, in activation of NOX2 and in mitochondrial ROS generation. Reactive Oxygen Species 14-17 cytochrome b-245, beta polypeptide Mus musculus 169-173 24104877-9 2014 CONCLUSION: These results suggest that the arrhythmogenic adverse effects of CGs on Ca(2+) handling involve PI3K- and PKC-mediated stimulation of NOX2 and subsequent NOX2-dependent ROS release from the mitochondria; mitochondria-derived ROS then activate CaMKII with consequent phosphorylation of RyR2 at Ser 2814. Reactive Oxygen Species 181-184 cytochrome b-245, beta polypeptide Mus musculus 166-170 25276054-9 2014 These data suggest that ROS derived from NADPH oxidases (mainly NOX1 and NOX2) and MAP kinase pathways could contribute to the induction and expansion of oxidative lesions characteristics of IBD and that apocynin could potentially be beneficial in IBD treatment. Reactive Oxygen Species 24-27 cytochrome b-245, beta polypeptide Mus musculus 73-77 24358357-2 2013 Previous work has shown that reactive oxygen species (ROS) produced by the superoxide generating enzyme NOX2/NADPH oxidase play a crucial role in the vascular pathology. Reactive Oxygen Species 29-52 cytochrome b-245, beta polypeptide Mus musculus 104-108 24358357-2 2013 Previous work has shown that reactive oxygen species (ROS) produced by the superoxide generating enzyme NOX2/NADPH oxidase play a crucial role in the vascular pathology. Reactive Oxygen Species 54-57 cytochrome b-245, beta polypeptide Mus musculus 104-108 24358357-11 2013 CONCLUSION: NOX2-generated ROS produced by both bone marrow-derived cells and resident retinal cells contribute importantly to retinal vascular injury in the diabetic retina. Reactive Oxygen Species 27-30 cytochrome b-245, beta polypeptide Mus musculus 12-16 24358335-1 2013 The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. Reactive Oxygen Species 65-88 cytochrome b-245, beta polypeptide Mus musculus 21-25 24358335-1 2013 The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. Reactive Oxygen Species 90-93 cytochrome b-245, beta polypeptide Mus musculus 4-19 24358335-1 2013 The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. Reactive Oxygen Species 90-93 cytochrome b-245, beta polypeptide Mus musculus 21-25 24014678-10 2013 Blockade of EP1R and Nox2-derived ROS inhibited ANG II and PGE2-mediated Ca(2+) currents. Reactive Oxygen Species 34-37 cytochrome b-245, beta polypeptide Mus musculus 21-25 24077950-2 2013 We showed a role for KATP channel, caveolae (caveolin-1), and NADPH oxidase 2 (NOX2) in ROS production with stop of flow. Reactive Oxygen Species 88-91 cytochrome b-245, beta polypeptide Mus musculus 62-77 24077950-2 2013 We showed a role for KATP channel, caveolae (caveolin-1), and NADPH oxidase 2 (NOX2) in ROS production with stop of flow. Reactive Oxygen Species 88-91 cytochrome b-245, beta polypeptide Mus musculus 79-83 24014678-11 2013 We propose a mechanism whereby ANG II increases COX-1-derived PGE2 through the AT1R/PLA2 pathway, which promotes ROS production by EP1R/Nox2 signaling in the SFO. Reactive Oxygen Species 113-116 cytochrome b-245, beta polypeptide Mus musculus 136-140 23918694-3 2013 The objectives of this study were to characterize and establish AIA as a model for periarticular bone loss, and to determine the importance of NADPH oxidase 2 (NOX-2)-derived reactive oxygen species (ROS) in periarticular bone loss. Reactive Oxygen Species 175-198 cytochrome b-245, beta polypeptide Mus musculus 143-158 23918694-3 2013 The objectives of this study were to characterize and establish AIA as a model for periarticular bone loss, and to determine the importance of NADPH oxidase 2 (NOX-2)-derived reactive oxygen species (ROS) in periarticular bone loss. Reactive Oxygen Species 175-198 cytochrome b-245, beta polypeptide Mus musculus 160-165 23918694-3 2013 The objectives of this study were to characterize and establish AIA as a model for periarticular bone loss, and to determine the importance of NADPH oxidase 2 (NOX-2)-derived reactive oxygen species (ROS) in periarticular bone loss. Reactive Oxygen Species 200-203 cytochrome b-245, beta polypeptide Mus musculus 160-165 23918694-10 2013 However, induction of arthritis in Ncf1 / mice, which lack NOX-2-derived ROS, and control mice resulted in similar reductions in periarticular trabecular BMD. Reactive Oxygen Species 73-76 cytochrome b-245, beta polypeptide Mus musculus 59-64 23918694-12 2013 Furthermore, based on our observations using this model, we conclude that NOX-2-derived ROS production is not essential for inflammation-mediated periarticular bone loss. Reactive Oxygen Species 88-91 cytochrome b-245, beta polypeptide Mus musculus 74-79 23957783-8 2013 CONCLUSIONS AND IMPLICATIONS: In conclusion, Nox2-derived ROS played a key role in damaging insulin receptor and endothelial function in dietary obesity after middle-age. Reactive Oxygen Species 58-61 cytochrome b-245, beta polypeptide Mus musculus 45-49 24039718-9 2013 Nox-2 and Nox-4 proteins are sources of ROS in blue light irradiated photoreceptors; the Nox inhibitor apocynin decreased ROS stimulated by blue light. Reactive Oxygen Species 40-43 cytochrome b-245, beta polypeptide Mus musculus 0-5 24241266-1 2013 An essential component of NAD(P)H, gp91phox, maintains the functionality of the enzyme in producing oxygen radicals. Reactive Oxygen Species 100-115 cytochrome b-245, beta polypeptide Mus musculus 35-43 23933064-8 2013 Knockdown of NOX2 and NOX4, using specific siRNA, reduced both basal and S1P-induced ROS formation. Reactive Oxygen Species 85-88 cytochrome b-245, beta polypeptide Mus musculus 13-17 24106122-10 2013 CONCLUSIONS: The Nox2-generated reactive oxygen species (ROS) facilitate the retinal expression of VEGF-A and neovascularization in this mouse model of OIR. Reactive Oxygen Species 32-55 cytochrome b-245, beta polypeptide Mus musculus 17-21 24106122-10 2013 CONCLUSIONS: The Nox2-generated reactive oxygen species (ROS) facilitate the retinal expression of VEGF-A and neovascularization in this mouse model of OIR. Reactive Oxygen Species 57-60 cytochrome b-245, beta polypeptide Mus musculus 17-21 23856052-3 2013 NADPH oxidase with Nox2 as the catalytic subunit is a major source for cardiac ROS production. Reactive Oxygen Species 79-82 cytochrome b-245, beta polypeptide Mus musculus 19-23 24018842-4 2013 We have generated a novel binary (Tet-ON/OFF) conditional transgenic mouse (Tet-Nox2:VE-Cad-tTA) that induces endothelial cell (EC)-specific overexpression of Nox2/gp91 (NADPH oxidase) and 1.8?0.42-fold increase in EC-ROS upon tetracycline withdrawal (Tet-OFF). Reactive Oxygen Species 218-221 cytochrome b-245, beta polypeptide Mus musculus 159-163 23857584-0 2013 FcgammaR-driven release of IL-6 by macrophages requires NOX2-dependent production of reactive oxygen species. Reactive Oxygen Species 85-108 cytochrome b-245, beta polypeptide Mus musculus 56-60 23857584-4 2013 We hypothesized that NOX2 generated ROS is necessary for propagation of downstream FcgammaR signaling and initiation of the innate immune response. Reactive Oxygen Species 36-39 cytochrome b-245, beta polypeptide Mus musculus 21-25 23857584-7 2013 Macrophages lacking the gp91(phox) subunit of NOX2 fail to produce ROS upon FcgammaR ligation, resulting in decreased Akt phosphorylation and a reduction in the levels of IL-6 compared with wild type macrophages. Reactive Oxygen Species 67-70 cytochrome b-245, beta polypeptide Mus musculus 46-50 23805104-2 2013 Many of the vascular effects of angiotensin II are mediated by reactive oxygen species (ROS) generated from homologs of NADPH oxidase with Nox2 predominating in small arteries and arterioles. Reactive Oxygen Species 63-86 cytochrome b-245, beta polypeptide Mus musculus 139-143 23554457-7 2013 In mitral valves from SOD1-deficient mice, expression of CTGF, MMP2, Nox2, and Nox4 was significantly increased, suggesting that ROS can independently activate pro-fibrotic and matrix remodelling gene expression patterns. Reactive Oxygen Species 129-132 cytochrome b-245, beta polypeptide Mus musculus 69-73 23459072-2 2013 We have reported that nitric oxide (NO) decreases reactive oxygen species production by endothelial Nox2. Reactive Oxygen Species 50-73 cytochrome b-245, beta polypeptide Mus musculus 100-104 23459072-4 2013 Specifically, we examined the influence of two well-characterized HNO donors, Angeli"s salt and isopropylamine NONOate (IPA/NO), on Nox2-dependent responses to angiotensin II (reactive oxygen species production and vasoconstriction) in mouse cerebral arteries. Reactive Oxygen Species 176-199 cytochrome b-245, beta polypeptide Mus musculus 132-136 23805104-2 2013 Many of the vascular effects of angiotensin II are mediated by reactive oxygen species (ROS) generated from homologs of NADPH oxidase with Nox2 predominating in small arteries and arterioles. Reactive Oxygen Species 88-91 cytochrome b-245, beta polypeptide Mus musculus 139-143 23536230-11 2013 Although LPS increased microglial activation and ROS at all ages studied, saline control NOX2(+/+) mice showed age-related increases in microglial activation, NOX, and ROS levels at 12 and 22 months of age. Reactive Oxygen Species 168-171 cytochrome b-245, beta polypeptide Mus musculus 89-93 23635512-3 2013 NOX2 (NADPH oxidase 2)-derived reactive oxygen species are critical for killing of certain pathogens by polymorphonuclear leukocytes (PMN). Reactive Oxygen Species 31-54 cytochrome b-245, beta polypeptide Mus musculus 0-4 23589615-5 2013 We observed that, in SOD1-G93A microglia, the stimulation of P2X7 receptor by 2"-3"-O-(benzoyl-benzoyl) ATP enhanced NOX2 activity in terms of translocation of p67(phox) to the membrane and ROS production; this effect was totally dependent on Rac1. Reactive Oxygen Species 190-193 cytochrome b-245, beta polypeptide Mus musculus 117-121 23589615-3 2013 The ALS-causing mutant protein Cu(+)/Zn(+) superoxide dismutase SOD1-G93A directly enhances the activity of the main ROS-producing enzyme in microglia, NADPH oxidase 2 (NOX2), a well-known player in the pathogenesis of ALS. Reactive Oxygen Species 117-120 cytochrome b-245, beta polypeptide Mus musculus 152-167 23589615-3 2013 The ALS-causing mutant protein Cu(+)/Zn(+) superoxide dismutase SOD1-G93A directly enhances the activity of the main ROS-producing enzyme in microglia, NADPH oxidase 2 (NOX2), a well-known player in the pathogenesis of ALS. Reactive Oxygen Species 117-120 cytochrome b-245, beta polypeptide Mus musculus 169-173 24371447-1 2013 During an infection, lipopolysaccharide (LPS) stimulates the production of reactive oxygen species (ROS), which is mediated, in large part, by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs); NOX2 is the major NOX isoform found in the macrophage cell membrane. Reactive Oxygen Species 75-98 cytochrome b-245, beta polypeptide Mus musculus 212-216 24371447-1 2013 During an infection, lipopolysaccharide (LPS) stimulates the production of reactive oxygen species (ROS), which is mediated, in large part, by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs); NOX2 is the major NOX isoform found in the macrophage cell membrane. Reactive Oxygen Species 100-103 cytochrome b-245, beta polypeptide Mus musculus 212-216 24371447-2 2013 While the immunomodulatory activity of propofol is highly documented, its effect on the LPS-induced NOX2/ROS/NF-kappaB signaling pathway in macrophages has not been addressed. Reactive Oxygen Species 105-108 cytochrome b-245, beta polypeptide Mus musculus 100-104 23635512-3 2013 NOX2 (NADPH oxidase 2)-derived reactive oxygen species are critical for killing of certain pathogens by polymorphonuclear leukocytes (PMN). Reactive Oxygen Species 31-54 cytochrome b-245, beta polypeptide Mus musculus 6-21 23171450-8 2012 These results clearly indicate that nicotinamide adenine dinucleotide phosphate oxidase is activated by gp91phox, which is expressed on the surface in response to the increased expression of hyaluronic acid induced by UVB irradiation, and as result, the generation of reactive oxygen species (ROS) increases. Reactive Oxygen Species 268-291 cytochrome b-245, beta polypeptide Mus musculus 104-112 23171450-8 2012 These results clearly indicate that nicotinamide adenine dinucleotide phosphate oxidase is activated by gp91phox, which is expressed on the surface in response to the increased expression of hyaluronic acid induced by UVB irradiation, and as result, the generation of reactive oxygen species (ROS) increases. Reactive Oxygen Species 293-296 cytochrome b-245, beta polypeptide Mus musculus 104-112 23024271-3 2012 While the early production of ROS (0-2 h) was dependent on the Nox2 isoform of NADPH oxidase, at later stages of B cell activation (6-24 h) ROS were generated by a second pathway, which appeared to be dependent on mitochondrial respiration. Reactive Oxygen Species 30-33 cytochrome b-245, beta polypeptide Mus musculus 63-67 23000198-1 2012 Reactive oxygen species (ROS) generated by Nox2 oxidase are reported to contribute to infarct damage following cerebral ischemia-reperfusion. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 43-47 23000198-1 2012 Reactive oxygen species (ROS) generated by Nox2 oxidase are reported to contribute to infarct damage following cerebral ischemia-reperfusion. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 43-47 23000198-6 2012 Our data therefore suggest that ROS production by Nox2 oxidase activity plays no significant role in the pathophysiology of cerebral ischemia in the absence of reperfusion. Reactive Oxygen Species 32-35 cytochrome b-245, beta polypeptide Mus musculus 50-54 22933115-10 2012 This study ascribes a new role for NOX2 in pancreatic beta-cells as negative modulator of the secretory response, reducing cAMP/PKA signaling secondary to ROS generation. Reactive Oxygen Species 155-158 cytochrome b-245, beta polypeptide Mus musculus 35-39 22933115-0 2012 NADPH oxidase NOX2 defines a new antagonistic role for reactive oxygen species and cAMP/PKA in the regulation of insulin secretion. Reactive Oxygen Species 55-78 cytochrome b-245, beta polypeptide Mus musculus 14-18 23024271-4 2012 B cells from mice deficient in the Nox2 NADPH oxidase complex lacked detectable early production of extracellular and intracellular ROS after BCR stimulation but had normal proximal BCR signaling and BCR-induced activation and proliferation in vitro and mounted normal or somewhat elevated Ab responses in vivo. Reactive Oxygen Species 132-135 cytochrome b-245, beta polypeptide Mus musculus 35-39 22648949-8 2012 Fibers from NOX2 knockout mice lacked ROS production and ROS-dependent nuclear efflux of HDAC5-GFP or HDAC4-GFP during 50-Hz trains but had unmodified Ca(2+) transients. Reactive Oxygen Species 38-41 cytochrome b-245, beta polypeptide Mus musculus 12-16 22685019-1 2012 Chronic granulomatous disease (CGD), caused by a lack of reactive oxygen species (ROS) generation by the phagocyte NADPH oxidase NOX2, leads to massively increased inflammatory responses. Reactive Oxygen Species 57-80 cytochrome b-245, beta polypeptide Mus musculus 31-34 22685019-1 2012 Chronic granulomatous disease (CGD), caused by a lack of reactive oxygen species (ROS) generation by the phagocyte NADPH oxidase NOX2, leads to massively increased inflammatory responses. Reactive Oxygen Species 57-80 cytochrome b-245, beta polypeptide Mus musculus 129-133 22911512-4 2012 In this study, we test the hypothesis that NADPH oxidase 2 (NOX2)-derived ROS may play a key role in dysfunction and apoptosis of pancreatic beta-cell induced by VLDL. Reactive Oxygen Species 74-77 cytochrome b-245, beta polypeptide Mus musculus 43-58 22911512-4 2012 In this study, we test the hypothesis that NADPH oxidase 2 (NOX2)-derived ROS may play a key role in dysfunction and apoptosis of pancreatic beta-cell induced by VLDL. Reactive Oxygen Species 74-77 cytochrome b-245, beta polypeptide Mus musculus 60-64 22911512-6 2012 In vitro, the treatment of pancreatic NIT-1 cells with 1 mg/ml VLDL for 12 h stimulated NOX2-derived ROS generation, decreased expression and secretion of insulin. Reactive Oxygen Species 101-104 cytochrome b-245, beta polypeptide Mus musculus 88-92 22911512-8 2012 In conclusion, our data demonstrate a critical role of NOX2-derived ROS in dysfunction and apoptosis through JNK and p53 pathways in pancreatic beta-cells induced by VLDL. Reactive Oxygen Species 68-71 cytochrome b-245, beta polypeptide Mus musculus 55-59 22685019-1 2012 Chronic granulomatous disease (CGD), caused by a lack of reactive oxygen species (ROS) generation by the phagocyte NADPH oxidase NOX2, leads to massively increased inflammatory responses. Reactive Oxygen Species 82-85 cytochrome b-245, beta polypeptide Mus musculus 31-34 22685019-1 2012 Chronic granulomatous disease (CGD), caused by a lack of reactive oxygen species (ROS) generation by the phagocyte NADPH oxidase NOX2, leads to massively increased inflammatory responses. Reactive Oxygen Species 82-85 cytochrome b-245, beta polypeptide Mus musculus 129-133 22685019-7 2012 Measurements of ROS in rescue mice demonstrated functional NOX2 in mononuclear phagocytes (macrophages and dendritic cells) but not in neutrophils. Reactive Oxygen Species 16-19 cytochrome b-245, beta polypeptide Mus musculus 59-63 22648949-0 2012 NOX2-dependent ROS is required for HDAC5 nuclear efflux and contributes to HDAC4 nuclear efflux during intense repetitive activity of fast skeletal muscle fibers. Reactive Oxygen Species 15-18 cytochrome b-245, beta polypeptide Mus musculus 0-4 22648949-8 2012 Fibers from NOX2 knockout mice lacked ROS production and ROS-dependent nuclear efflux of HDAC5-GFP or HDAC4-GFP during 50-Hz trains but had unmodified Ca(2+) transients. Reactive Oxygen Species 57-60 cytochrome b-245, beta polypeptide Mus musculus 12-16 22648949-9 2012 Our results demonstrate that ROS generated by NOX2 could play important roles in muscle remodeling due to intense muscle activity and that the nuclear effluxes of HDAC4 and HDAC5 are differentially regulated by Ca(2+) and ROS during muscle activity. Reactive Oxygen Species 29-32 cytochrome b-245, beta polypeptide Mus musculus 46-50 22648949-9 2012 Our results demonstrate that ROS generated by NOX2 could play important roles in muscle remodeling due to intense muscle activity and that the nuclear effluxes of HDAC4 and HDAC5 are differentially regulated by Ca(2+) and ROS during muscle activity. Reactive Oxygen Species 222-225 cytochrome b-245, beta polypeptide Mus musculus 46-50 22572846-4 2012 ROS production depends on NADPH oxidase (NOX2), the activity of which requires continuous pH and charge compensation. Reactive Oxygen Species 0-3 cytochrome b-245, beta polypeptide Mus musculus 41-45 22146192-8 2012 These results strongly suggest that NOX2 activation releases reactive oxygen species after CK2 inhibition, triggering release of apoptogenic factors from mitochondria and inducing DNA damage after ischemic brain injury. Reactive Oxygen Species 61-84 cytochrome b-245, beta polypeptide Mus musculus 36-40 22726689-8 2012 Thus, ebselen and its analogs represent a class of compounds that inhibit ROS generation by interrupting the assembly of Nox2-activating regulatory subunits. Reactive Oxygen Species 74-77 cytochrome b-245, beta polypeptide Mus musculus 121-125 22491245-0 2012 Reactive oxygen species produced by the NADPH oxidase 2 complex in monocytes protect mice from bacterial infections. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 40-55 22491245-2 2012 CGD results from defective production of reactive oxygen species by phagocytes caused by mutations in genes encoding the NADPH oxidase 2 (NOX2) complex subunits. Reactive Oxygen Species 41-64 cytochrome b-245, beta polypeptide Mus musculus 121-136 22491245-2 2012 CGD results from defective production of reactive oxygen species by phagocytes caused by mutations in genes encoding the NADPH oxidase 2 (NOX2) complex subunits. Reactive Oxygen Species 41-64 cytochrome b-245, beta polypeptide Mus musculus 138-142 22290850-2 2012 We demonstrated that NADPH oxidase 2 (Nox2)-derived reactive oxygen species (ROS) are involved in postischemic mobilization of BM cells and revascularization. Reactive Oxygen Species 52-75 cytochrome b-245, beta polypeptide Mus musculus 21-36 22290850-2 2012 We demonstrated that NADPH oxidase 2 (Nox2)-derived reactive oxygen species (ROS) are involved in postischemic mobilization of BM cells and revascularization. Reactive Oxygen Species 52-75 cytochrome b-245, beta polypeptide Mus musculus 38-42 22290850-2 2012 We demonstrated that NADPH oxidase 2 (Nox2)-derived reactive oxygen species (ROS) are involved in postischemic mobilization of BM cells and revascularization. Reactive Oxygen Species 77-80 cytochrome b-245, beta polypeptide Mus musculus 21-36 22290850-2 2012 We demonstrated that NADPH oxidase 2 (Nox2)-derived reactive oxygen species (ROS) are involved in postischemic mobilization of BM cells and revascularization. Reactive Oxygen Species 77-80 cytochrome b-245, beta polypeptide Mus musculus 38-42 22290850-4 2012 Here, we show that hindlimb ischemia of mice increases ROS production in both the endosteal and central region of BM tissue in situ, which is almost completely abolished in Nox2 knockout (KO) mice. Reactive Oxygen Species 55-58 cytochrome b-245, beta polypeptide Mus musculus 173-177 22290850-5 2012 This Nox2-dependent ROS production is mainly derived from Gr-1(+) myeloid cells in BM. Reactive Oxygen Species 20-23 cytochrome b-245, beta polypeptide Mus musculus 5-9 22290850-10 2012 In summary, Nox2-dependent increase in ROS plays a critical role in regulating hypoxia expansion and proteolytic activities in BM microenvironment in response to tissue ischemia. Reactive Oxygen Species 39-42 cytochrome b-245, beta polypeptide Mus musculus 12-16 22642907-1 2012 The suppressive role of phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) complex-derived reactive oxygen species (ROS) in adaptive immunity-driven arthritis models is well established. Reactive Oxygen Species 117-140 cytochrome b-245, beta polypeptide Mus musculus 95-99 22642907-1 2012 The suppressive role of phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) complex-derived reactive oxygen species (ROS) in adaptive immunity-driven arthritis models is well established. Reactive Oxygen Species 142-145 cytochrome b-245, beta polypeptide Mus musculus 95-99 22642907-2 2012 In this study, we aimed to investigate the role of NOX2 complex-derived ROS in a model of innate immunity-driven arthritis and to identify the ROS-regulated innate receptors that control arthritis. Reactive Oxygen Species 72-75 cytochrome b-245, beta polypeptide Mus musculus 51-55 22505671-12 2012 We conclude that acid-induced ALI causes NOX2-mediated ROS generation that activates platelets, which then generate a procoagulant endothelial surface. Reactive Oxygen Species 55-58 cytochrome b-245, beta polypeptide Mus musculus 41-45 22056415-2 2012 Studies from mice lacking Hv1 channels showed that Hv1 proton channels are required for high-level production of reactive oxygen species (ROS) by the NADPH oxidase of phagocytes (NOX2) in two ways. Reactive Oxygen Species 113-136 cytochrome b-245, beta polypeptide Mus musculus 179-183 22056415-2 2012 Studies from mice lacking Hv1 channels showed that Hv1 proton channels are required for high-level production of reactive oxygen species (ROS) by the NADPH oxidase of phagocytes (NOX2) in two ways. Reactive Oxygen Species 138-141 cytochrome b-245, beta polypeptide Mus musculus 179-183 22814241-0 2012 NADPH oxidase 2-derived reactive oxygen species are involved in dysfunction and apoptosis of pancreatic beta-cells induced by low density lipoprotein. Reactive Oxygen Species 24-47 cytochrome b-245, beta polypeptide Mus musculus 0-15 22140041-10 2012 In cultured PVN neurons, silencing either NOX2 or NOX4 protein production by culturing PVN cells with siRNA-NOX2 or siRNA-NOX4 attenuated Aldo-induced ROS. Reactive Oxygen Species 151-154 cytochrome b-245, beta polypeptide Mus musculus 42-46 22140041-10 2012 In cultured PVN neurons, silencing either NOX2 or NOX4 protein production by culturing PVN cells with siRNA-NOX2 or siRNA-NOX4 attenuated Aldo-induced ROS. Reactive Oxygen Species 151-154 cytochrome b-245, beta polypeptide Mus musculus 108-112 22399808-9 2012 Conversely, reactive oxygen species derived from NOX2 were required for U-II activation of HIF and upregulation of HIF-1. Reactive Oxygen Species 12-35 cytochrome b-245, beta polypeptide Mus musculus 49-53 22221582-8 2012 The ability of tempol to attenuate cardiac hypertrophy suggests that a cytosolic source of reactive oxygen species, probably NOX2, may contribute to the hypertrophic phenotype in G4H(-/-) mice. Reactive Oxygen Species 91-114 cytochrome b-245, beta polypeptide Mus musculus 125-129 22337127-5 2012 Production of reactive oxygen species was completely abolished in Nox2(y/-) cells. Reactive Oxygen Species 14-37 cytochrome b-245, beta polypeptide Mus musculus 66-70 22814241-12 2012 CONCLUSIONS: NOX2-derived ROS may play a key role in LDL-induced dysfunction and apoptosis of pancreatic beta-cells through JNK and p53 pathways. Reactive Oxygen Species 26-29 cytochrome b-245, beta polypeptide Mus musculus 13-17 23118986-1 2012 Nox2 oxidase is one isoform in a family of seven NADPH oxidases that generate reactive oxygen species (ROS) and thereby contribute to physiological and pathological processes including host defense, redox signaling and oxidative tissue damage. Reactive Oxygen Species 78-101 cytochrome b-245, beta polypeptide Mus musculus 0-4 23118986-1 2012 Nox2 oxidase is one isoform in a family of seven NADPH oxidases that generate reactive oxygen species (ROS) and thereby contribute to physiological and pathological processes including host defense, redox signaling and oxidative tissue damage. Reactive Oxygen Species 103-106 cytochrome b-245, beta polypeptide Mus musculus 0-4 21896326-1 2011 Production of reactive oxygen species (ROS) resulting from phagocytic NADPH oxidase (NOX2) activity has been reported to contribute to host defense against numerous microbial pathogens. Reactive Oxygen Species 14-37 cytochrome b-245, beta polypeptide Mus musculus 85-89 21251215-12 2011 Nox2 and Nox4 siRNA significantly attenuated TNF-alpha-induced ROS and upregulation of IL-1beta and IL-6 in cardiomyocytes. Reactive Oxygen Species 63-66 cytochrome b-245, beta polypeptide Mus musculus 0-4 21896326-1 2011 Production of reactive oxygen species (ROS) resulting from phagocytic NADPH oxidase (NOX2) activity has been reported to contribute to host defense against numerous microbial pathogens. Reactive Oxygen Species 39-42 cytochrome b-245, beta polypeptide Mus musculus 85-89 21896326-8 2011 Although NOX2-derived ROS appeared to be dispensable for both innate and acquired immunity to pulmonary Coccidioides infection, evidence is presented that NOX2 production plays a role in limiting pathogenic inflammation in this murine model of coccidioidomycosis. Reactive Oxygen Species 22-25 cytochrome b-245, beta polypeptide Mus musculus 9-13 21937428-1 2011 Recent studies have implicated enhanced Nox2-mediated reactive oxygen species (ROS) by microglia in the pathogenesis of motor neuron death observed in familial amyotrophic lateral sclerosis (ALS). Reactive Oxygen Species 54-77 cytochrome b-245, beta polypeptide Mus musculus 40-44 21937428-1 2011 Recent studies have implicated enhanced Nox2-mediated reactive oxygen species (ROS) by microglia in the pathogenesis of motor neuron death observed in familial amyotrophic lateral sclerosis (ALS). Reactive Oxygen Species 79-82 cytochrome b-245, beta polypeptide Mus musculus 40-44 21937428-8 2011 SOD1(G93A) expression enhanced recruitment of alsin to the endomembrane compartment in glial cells, suggesting that these two proteins act to modulate Nox2-dependent endosomal ROS and proinflammatory signals that modulate NFkappaB. Reactive Oxygen Species 176-179 cytochrome b-245, beta polypeptide Mus musculus 151-155 21937428-2 2011 In this context, ALS mutant forms of SOD1 enhance Rac1 activation, leading to increased Nox2-dependent microglial ROS production and neuron cell death in mice. Reactive Oxygen Species 114-117 cytochrome b-245, beta polypeptide Mus musculus 88-92 21911606-6 2011 Thus, ST2-deficient mice exhibit an increased susceptibility to polymicrobial infection with impaired bacterial clearance, which is associated with defects in phagosome maturation and NOX2-derived production of reactive oxygen species characterized in ST2-deficient phagocytes. Reactive Oxygen Species 211-234 cytochrome b-245, beta polypeptide Mus musculus 184-188 21302291-2 2011 Cardiovascular morbidities caused by IH are triggered by increased generation of reactive oxygen species (ROS) by pro-oxidant enzymes, especially NADPH oxidase-2 (Nox2). Reactive Oxygen Species 81-104 cytochrome b-245, beta polypeptide Mus musculus 146-161 21302291-2 2011 Cardiovascular morbidities caused by IH are triggered by increased generation of reactive oxygen species (ROS) by pro-oxidant enzymes, especially NADPH oxidase-2 (Nox2). Reactive Oxygen Species 81-104 cytochrome b-245, beta polypeptide Mus musculus 163-167 21302291-2 2011 Cardiovascular morbidities caused by IH are triggered by increased generation of reactive oxygen species (ROS) by pro-oxidant enzymes, especially NADPH oxidase-2 (Nox2). Reactive Oxygen Species 106-109 cytochrome b-245, beta polypeptide Mus musculus 146-161 21302291-2 2011 Cardiovascular morbidities caused by IH are triggered by increased generation of reactive oxygen species (ROS) by pro-oxidant enzymes, especially NADPH oxidase-2 (Nox2). Reactive Oxygen Species 106-109 cytochrome b-245, beta polypeptide Mus musculus 163-167 22002428-0 2011 Activation of NOX2 by the stimulation of ionotropic and metabotropic glutamate receptors contributes to glutamate neurotoxicity in vivo through the production of reactive oxygen species and calpain activation. Reactive Oxygen Species 162-185 cytochrome b-245, beta polypeptide Mus musculus 14-18 22002428-7 2011 By contrast, mice lacking NOX2 were less vulnerable to excitotoxicity, and there was reduced ROS production and protein nitrosylation, microglial reactivity, and calpain activation. Reactive Oxygen Species 93-96 cytochrome b-245, beta polypeptide Mus musculus 26-30 22002428-9 2011 Neuronal damage involves ROS production by NOX2, which, in turn, contributes to calpain activation. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 43-47 21636565-1 2011 We previously reported that reactive oxygen species generated by NADPH oxidase 2 (Nox2) induces sensory plasticity of the carotid body, manifested as a progressive increase in baseline sensory activity or sensory long-term facilitation (sLTF). Reactive Oxygen Species 28-51 cytochrome b-245, beta polypeptide Mus musculus 65-80 21636565-1 2011 We previously reported that reactive oxygen species generated by NADPH oxidase 2 (Nox2) induces sensory plasticity of the carotid body, manifested as a progressive increase in baseline sensory activity or sensory long-term facilitation (sLTF). Reactive Oxygen Species 28-51 cytochrome b-245, beta polypeptide Mus musculus 82-86 21636565-8 2011 Reactive oxygen species levels increased in response to repetitive applications of ANG II, and this effect was blocked by apocynin, an inhibitor of Nox2, as well as losartan, an angiotensin type 1 (AT(1)) receptor antagonist. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 148-152 21512969-6 2011 In BV-2 cells, OGD induced ROS and nitric oxide production by upregulating NOX2 and iNOS via the phosphatidylinositol-3-kinase (PI3K)/AKT-dependent NF- kappaB and HIF-1 alpha pathways, and these changes were suppressed by andrographolide and LY294002. Reactive Oxygen Species 27-30 cytochrome b-245, beta polypeptide Mus musculus 75-79 21903813-1 2011 We report that in heart cells, physiologic stretch rapidly activates reduced-form nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) to produce reactive oxygen species (ROS) in a process dependent on microtubules (X-ROS signaling). Reactive Oxygen Species 162-185 cytochrome b-245, beta polypeptide Mus musculus 82-143 21903813-1 2011 We report that in heart cells, physiologic stretch rapidly activates reduced-form nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) to produce reactive oxygen species (ROS) in a process dependent on microtubules (X-ROS signaling). Reactive Oxygen Species 162-185 cytochrome b-245, beta polypeptide Mus musculus 145-149 21903813-1 2011 We report that in heart cells, physiologic stretch rapidly activates reduced-form nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) to produce reactive oxygen species (ROS) in a process dependent on microtubules (X-ROS signaling). Reactive Oxygen Species 187-190 cytochrome b-245, beta polypeptide Mus musculus 82-143 21903813-1 2011 We report that in heart cells, physiologic stretch rapidly activates reduced-form nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) to produce reactive oxygen species (ROS) in a process dependent on microtubules (X-ROS signaling). Reactive Oxygen Species 187-190 cytochrome b-245, beta polypeptide Mus musculus 145-149 21903813-2 2011 ROS production occurs in the sarcolemmal and t-tubule membranes where NOX2 is located and sensitizes nearby ryanodine receptors (RyRs) in the sarcoplasmic reticulum (SR). Reactive Oxygen Species 0-3 cytochrome b-245, beta polypeptide Mus musculus 70-74 21664456-0 2011 Nox2-derived ROS in PPARgamma signaling and cell-cycle progression of lung alveolar epithelial cells. Reactive Oxygen Species 13-16 cytochrome b-245, beta polypeptide Mus musculus 0-4 21524749-0 2011 Nox2-derived reactive oxygen species contribute to hypercholesterolemia-induced inhibition of neovascularization: effects on endothelial progenitor cells and mature endothelial cells. Reactive Oxygen Species 13-36 cytochrome b-245, beta polypeptide Mus musculus 0-4 21524749-3 2011 Here we investigated the role of Nox2-derived reactive oxygen species (ROS) in the modulation of neovascularization by hypercholesterolemia. Reactive Oxygen Species 46-69 cytochrome b-245, beta polypeptide Mus musculus 33-37 21524749-3 2011 Here we investigated the role of Nox2-derived reactive oxygen species (ROS) in the modulation of neovascularization by hypercholesterolemia. Reactive Oxygen Species 71-74 cytochrome b-245, beta polypeptide Mus musculus 33-37 21524749-9 2011 In vitro, HUVECs treated with the NADPH oxidase inhibitor apocynin or endothelial cells isolated from the aorta of Nox2(-/-) mice exhibited reduced ROS formation following exposure to oxLDL. Reactive Oxygen Species 148-151 cytochrome b-245, beta polypeptide Mus musculus 115-119 21664456-7 2011 In conclusion, PPARgamma activation through Nox2-derived ROS promotes cell-cycle progression in normal mouse lungs and in cultured normal alveolar epithelial cells. Reactive Oxygen Species 57-60 cytochrome b-245, beta polypeptide Mus musculus 44-48 21615929-1 2011 BACKGROUND: Nox-2 (also known as gp91phox), a subunit component of NADPH oxidases, generates reactive oxygen species (ROS). Reactive Oxygen Species 93-116 cytochrome b-245, beta polypeptide Mus musculus 12-17 21606175-1 2011 The NADPH oxidase (Nox) subunits 1, 2 (gp91 phox), and 4 are the major sources for reactive oxygen species (ROS) in vascular tissues. Reactive Oxygen Species 83-106 cytochrome b-245, beta polypeptide Mus musculus 39-48 21606175-1 2011 The NADPH oxidase (Nox) subunits 1, 2 (gp91 phox), and 4 are the major sources for reactive oxygen species (ROS) in vascular tissues. Reactive Oxygen Species 108-111 cytochrome b-245, beta polypeptide Mus musculus 39-48 21606175-9 2011 In conclusion, A(3)AR enhances ROS generation, possibly through activation of Nox2, with subsequent contraction of the mouse aorta. Reactive Oxygen Species 31-34 cytochrome b-245, beta polypeptide Mus musculus 78-82 21615929-1 2011 BACKGROUND: Nox-2 (also known as gp91phox), a subunit component of NADPH oxidases, generates reactive oxygen species (ROS). Reactive Oxygen Species 93-116 cytochrome b-245, beta polypeptide Mus musculus 33-41 21615929-1 2011 BACKGROUND: Nox-2 (also known as gp91phox), a subunit component of NADPH oxidases, generates reactive oxygen species (ROS). Reactive Oxygen Species 118-121 cytochrome b-245, beta polypeptide Mus musculus 12-17 21615929-1 2011 BACKGROUND: Nox-2 (also known as gp91phox), a subunit component of NADPH oxidases, generates reactive oxygen species (ROS). Reactive Oxygen Species 118-121 cytochrome b-245, beta polypeptide Mus musculus 33-41 21615929-5 2011 RESULTS: The present study showed that the increased ROS production and NO release in activated BV-2 microglial cells by LPS were associated with increased expression of Nox-2 and iNOS. Reactive Oxygen Species 53-56 cytochrome b-245, beta polypeptide Mus musculus 170-175 21615929-9 2011 The overexpression of MKP-1 or inhibition of MAPKs (by specific inhibitors of JNK and p38 MAPKs), were found to downregulate the expression of Nox-2 and iNOS and thereby inhibit the synthesis of ROS and NO in activated BV-2 cells. Reactive Oxygen Species 195-198 cytochrome b-245, beta polypeptide Mus musculus 143-148 21615929-11 2011 On the other hand, knockdown of Nox-2 in BV-2 cells suppressed the LPS-induced ROS production and NO release. Reactive Oxygen Species 79-82 cytochrome b-245, beta polypeptide Mus musculus 32-37 21372137-4 2011 Mct-1 knockdown also prevented IL-1beta-induced expression of phagocyte-type NADPH oxidase (NOX-2), an enzyme specialized for production of ROS, whereas it did not have an effect on inducible NO synthase. Reactive Oxygen Species 140-143 cytochrome b-245, beta polypeptide Mus musculus 92-97 21384410-12 2011 Both NOX1- and NOX2-deficient HSCs had decreased ROS generation and failed to up-regulate collagen alpha1(I) and transforming growth factor beta in response to angiotensin II. Reactive Oxygen Species 49-52 cytochrome b-245, beta polypeptide Mus musculus 15-19 21372137-11 2011 These results suggest that MCT-1 contributes to NOX-2 expression via late phase activation of NF-kappaB in a ROS-dependent manner in ATDC5 cells exposed to IL-1beta. Reactive Oxygen Species 109-112 cytochrome b-245, beta polypeptide Mus musculus 48-53 22145029-0 2011 NADPH oxidase-2 derived ROS dictates murine DC cytokine-mediated cell fate decisions during CD4 T helper-cell commitment. Reactive Oxygen Species 24-27 cytochrome b-245, beta polypeptide Mus musculus 0-15 21268010-5 2011 CIA severity is enhanced by a mutation in the Ncf1 gene, impairing reactive oxygen species (ROS) production by the phagocyte NADPH oxidase (NOX2) complex. Reactive Oxygen Species 67-90 cytochrome b-245, beta polypeptide Mus musculus 140-144 21268010-5 2011 CIA severity is enhanced by a mutation in the Ncf1 gene, impairing reactive oxygen species (ROS) production by the phagocyte NADPH oxidase (NOX2) complex. Reactive Oxygen Species 92-95 cytochrome b-245, beta polypeptide Mus musculus 140-144 21268010-9 2011 These findings demonstrate for the first time that macrophages can initiate arthritis and that the process is negatively regulated by ROS produced via the NOX2 complex. Reactive Oxygen Species 134-137 cytochrome b-245, beta polypeptide Mus musculus 155-159 22145029-5 2011 Increasing endogenous H(2)O(2) attenuates p38-MAPK activity in IFNgamma/LPS stimulated WT and p47(phox-/-) DC, which suggests that endogenous Nox 2-derived ROS functions as a secondary messenger in the activated p38-MAPK signaling pathway during IL-12 expression. Reactive Oxygen Species 156-159 cytochrome b-245, beta polypeptide Mus musculus 142-147 22145029-1 2011 NADPH oxidase-2 (Nox2)/gp91(phox) and p47(phox) deficient mice are prone to hyper-inflammatory responses suggesting a paradoxical role for Nox2-derived reactive oxygen species (ROS) as anti-inflammatory mediators. Reactive Oxygen Species 177-180 cytochrome b-245, beta polypeptide Mus musculus 0-15 22145029-1 2011 NADPH oxidase-2 (Nox2)/gp91(phox) and p47(phox) deficient mice are prone to hyper-inflammatory responses suggesting a paradoxical role for Nox2-derived reactive oxygen species (ROS) as anti-inflammatory mediators. Reactive Oxygen Species 177-180 cytochrome b-245, beta polypeptide Mus musculus 17-21 22145029-1 2011 NADPH oxidase-2 (Nox2)/gp91(phox) and p47(phox) deficient mice are prone to hyper-inflammatory responses suggesting a paradoxical role for Nox2-derived reactive oxygen species (ROS) as anti-inflammatory mediators. Reactive Oxygen Species 177-180 cytochrome b-245, beta polypeptide Mus musculus 139-143 22145029-4 2011 The Nox2-dependent ROS production in DC negatively regulates proinflammatory IL-12 expression in DC by constraining p38-MAPK activity. Reactive Oxygen Species 19-22 cytochrome b-245, beta polypeptide Mus musculus 4-8 21209957-0 2010 NADPH oxidase 2-derived reactive oxygen species mediate FFAs-induced dysfunction and apoptosis of beta-cells via JNK, p38 MAPK and p53 pathways. Reactive Oxygen Species 24-47 cytochrome b-245, beta polypeptide Mus musculus 0-15 21209957-5 2010 In the present study, we test the hypothesis that NOX2-derived ROS may play a critical role in dysfunction and apoptosis of beta-cells induced by FFA. Reactive Oxygen Species 63-66 cytochrome b-245, beta polypeptide Mus musculus 50-54 20940302-0 2010 Inactivation of adenosine A2A receptor attenuates basal and angiotensin II-induced ROS production by Nox2 in endothelial cells. Reactive Oxygen Species 83-86 cytochrome b-245, beta polypeptide Mus musculus 101-105 20940302-1 2010 Endothelial cells (ECs) express a Nox2 enzyme, which, by generating reactive oxygen species (ROS), contributes to EC redox signaling and angiotensin II (AngII)-induced endothelial dysfunction. Reactive Oxygen Species 68-91 cytochrome b-245, beta polypeptide Mus musculus 34-38 20952384-0 2010 Reactive oxygen species generated by NADPH oxidase 2 and 4 are required for chondrogenic differentiation. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 37-58 20940302-1 2010 Endothelial cells (ECs) express a Nox2 enzyme, which, by generating reactive oxygen species (ROS), contributes to EC redox signaling and angiotensin II (AngII)-induced endothelial dysfunction. Reactive Oxygen Species 93-96 cytochrome b-245, beta polypeptide Mus musculus 34-38 20952384-7 2010 Depletion of Nox2 or Nox4 expression by RNA interference blocked both ROS generation and differentiation of ATDC5 cells, whereas depletion of Nox1 had no such effect. Reactive Oxygen Species 70-73 cytochrome b-245, beta polypeptide Mus musculus 13-17 20940302-4 2010 In cultured ECs (SVEC4-10), AngII (100 nm, 30 min) significantly increased Nox2 membrane translocation and association with A(2A)R. These were accompanied by p47(phox), ERK1/2, p38 MAPK, and Akt phosphorylation and an increased ROS production (169 +- 0.04%). Reactive Oxygen Species 228-231 cytochrome b-245, beta polypeptide Mus musculus 75-79 20952384-11 2010 Taken together, our data suggest that ROS generated by Nox2 or Nox4 are essential for survival and differentiation in the early stage of chondrogenesis. Reactive Oxygen Species 38-41 cytochrome b-245, beta polypeptide Mus musculus 55-59 20940302-9 2010 In conclusion, A(2A)R is involved in the regulation of EC ROS production by Nox2. Reactive Oxygen Species 58-61 cytochrome b-245, beta polypeptide Mus musculus 76-80 21073655-7 2010 In vitro, increased ROS levels in pancreatic NIT-1 cells exposed to high concentrations of glucose (33.3 mmol L(-1)) were associated with elevated expression of NOX2. Reactive Oxygen Species 20-23 cytochrome b-245, beta polypeptide Mus musculus 161-165 21073655-10 2010 In conclusion, NOX2-derived ROS could play a critical role in high glucose-induced beta-cell dysfunction through PTEN-dependent JNK activation and AKT inhibition. Reactive Oxygen Species 28-31 cytochrome b-245, beta polypeptide Mus musculus 15-19 21073655-4 2010 Here, we demonstrate a key role of NADPH oxidase 2 (NOX2)-derived ROS in the deterioration of beta-cell function induced by a high concentration of glucose. Reactive Oxygen Species 66-69 cytochrome b-245, beta polypeptide Mus musculus 35-50 21073655-4 2010 Here, we demonstrate a key role of NADPH oxidase 2 (NOX2)-derived ROS in the deterioration of beta-cell function induced by a high concentration of glucose. Reactive Oxygen Species 66-69 cytochrome b-245, beta polypeptide Mus musculus 52-56 20826812-9 2010 These results suggest that LPS-mediated Srx induction is dependent on both AP-1 and Nrf2, which is regulated by Nox2-derived reactive oxygen species. Reactive Oxygen Species 125-148 cytochrome b-245, beta polypeptide Mus musculus 112-116 20884632-3 2010 In this study, we investigated contributions to doxorubicin cardiotoxicity from Nox2 NADPH oxidase, an important ROS source in cardiac cells, which is known to modulate several key processes underlying the myocardial response to injury. Reactive Oxygen Species 113-116 cytochrome b-245, beta polypeptide Mus musculus 80-84 20884632-10 2010 Our findings suggest that ROS specifically derived from Nox2 NADPH oxidase make a substantial contribution to several key processes underlying development of cardiac contractile dysfunction and remodeling associated with doxorubicin chemotherapy. Reactive Oxygen Species 26-29 cytochrome b-245, beta polypeptide Mus musculus 56-60 20627937-2 2010 We hypothesized that NOX2 deficiency decreases reactive oxygen species (ROS) production and immune response and protects against streptozotocin (STZ)-induced beta-cell destruction and development of diabetes in mice. Reactive Oxygen Species 47-70 cytochrome b-245, beta polypeptide Mus musculus 21-25 20627937-2 2010 We hypothesized that NOX2 deficiency decreases reactive oxygen species (ROS) production and immune response and protects against streptozotocin (STZ)-induced beta-cell destruction and development of diabetes in mice. Reactive Oxygen Species 72-75 cytochrome b-245, beta polypeptide Mus musculus 21-25 20627937-9 2010 CONCLUSIONS: NOX2 deficiency decreases beta-cell destruction and preserves islet function in STZ-induced diabetes by reducing ROS production, immune response, and beta-cell apoptosis. Reactive Oxygen Species 126-129 cytochrome b-245, beta polypeptide Mus musculus 13-17 20685364-13 2010 Based on reporter assays, production of NOX2-mediated reactive oxygen species directly induced collagen promoter activity in HSC. Reactive Oxygen Species 54-77 cytochrome b-245, beta polypeptide Mus musculus 40-44 20360249-2 2010 Yet macrophage deficiency of phagocytic NADPH oxidase (Nox2), the primary source of ROS in macrophages, does not reduce atherosclerotic lesion development in mice. Reactive Oxygen Species 84-87 cytochrome b-245, beta polypeptide Mus musculus 55-59 20679217-0 2010 NADPH oxidase 2-derived reactive oxygen species in spinal cord microglia contribute to peripheral nerve injury-induced neuropathic pain. Reactive Oxygen Species 24-47 cytochrome b-245, beta polypeptide Mus musculus 0-15 20679217-2 2010 Here, we provide evidence that NADPH oxidase 2 (Nox2)-derived ROS production plays a critical role in nerve injury-induced spinal cord microglia activation and subsequent pain hypersensitivity. Reactive Oxygen Species 62-65 cytochrome b-245, beta polypeptide Mus musculus 31-46 20679217-2 2010 Here, we provide evidence that NADPH oxidase 2 (Nox2)-derived ROS production plays a critical role in nerve injury-induced spinal cord microglia activation and subsequent pain hypersensitivity. Reactive Oxygen Species 62-65 cytochrome b-245, beta polypeptide Mus musculus 48-52 20679217-4 2010 Studies using Nox2-deficient mice show that Nox2 is required for SNT-induced ROS generation, microglia activation, and proinflammatory cytokine expression in the spinal cord. Reactive Oxygen Species 77-80 cytochrome b-245, beta polypeptide Mus musculus 44-48 20679217-8 2010 These studies delineate a pathway involving nerve damage leading to microglial Nox2-generated ROS, resulting in the expression of proinflammatory cytokines that are involved in the initiation of neuropathic pain. Reactive Oxygen Species 94-97 cytochrome b-245, beta polypeptide Mus musculus 79-83 20659322-12 2010 Modulating gp91phox and gp91phox -derived ROS may provide a new therapeutic strategy in combating post-traumatic brain injury. Reactive Oxygen Species 42-45 cytochrome b-245, beta polypeptide Mus musculus 24-32 20739552-2 2010 Subchronic administration of ketamine leads to loss of parvalbumin-positive interneurons through reactive oxygen species (ROS), generated by the NADPH oxidase NOX2. Reactive Oxygen Species 97-120 cytochrome b-245, beta polypeptide Mus musculus 159-163 20739552-2 2010 Subchronic administration of ketamine leads to loss of parvalbumin-positive interneurons through reactive oxygen species (ROS), generated by the NADPH oxidase NOX2. Reactive Oxygen Species 122-125 cytochrome b-245, beta polypeptide Mus musculus 159-163 20739552-8 2010 Our results suggest that NOX2 is a major source of ROS production in the prefrontal cortex controlling glutamate release and associated behavioral alterations after acute ketamine exposure. Reactive Oxygen Species 51-54 cytochrome b-245, beta polypeptide Mus musculus 25-29 19935767-1 2010 This study examined the hypothesis that the control of NADPH oxidase-2 (Nox2)-mediated reactive oxygen species (ROS) regulates the expression of matrix metalloproteinases (MMPs) and the migration of macrophages. Reactive Oxygen Species 87-110 cytochrome b-245, beta polypeptide Mus musculus 55-70 19935767-1 2010 This study examined the hypothesis that the control of NADPH oxidase-2 (Nox2)-mediated reactive oxygen species (ROS) regulates the expression of matrix metalloproteinases (MMPs) and the migration of macrophages. Reactive Oxygen Species 87-110 cytochrome b-245, beta polypeptide Mus musculus 72-76 19935767-1 2010 This study examined the hypothesis that the control of NADPH oxidase-2 (Nox2)-mediated reactive oxygen species (ROS) regulates the expression of matrix metalloproteinases (MMPs) and the migration of macrophages. Reactive Oxygen Species 112-115 cytochrome b-245, beta polypeptide Mus musculus 55-70 19935767-1 2010 This study examined the hypothesis that the control of NADPH oxidase-2 (Nox2)-mediated reactive oxygen species (ROS) regulates the expression of matrix metalloproteinases (MMPs) and the migration of macrophages. Reactive Oxygen Species 112-115 cytochrome b-245, beta polypeptide Mus musculus 72-76 20500986-2 2010 The NADPH oxidases are a family of ROS generating enzymes, of which four members (Nox1, Nox2, Nox4 and Nox5) are expressed in blood vessels. Reactive Oxygen Species 35-38 cytochrome b-245, beta polypeptide Mus musculus 88-92 19837950-6 2010 Nox2 expression was upregulated in the aortic endothelium of ApoE(-/-) mice before the appearance of lesions, and this was associated with elevated ROS levels. Reactive Oxygen Species 148-151 cytochrome b-245, beta polypeptide Mus musculus 0-4 19837950-9 2010 However, an en face examination of the aorta from the arch to the iliac bifurcation revealed a 50% reduction in lesion area in Nox2(-/y)/ApoE(-/-) versus ApoE(-/-) mice, and this was associated with a marked decrease in aortic ROS production and an increased NO bioavailability. Reactive Oxygen Species 227-230 cytochrome b-245, beta polypeptide Mus musculus 127-131 19837950-10 2010 In conclusion, this is the first demonstration of a role for Nox2-NADPH oxidase in vascular ROS production, reduced NO bioavailability, and early lesion development in ApoE(-/-) mice, highlighting this Nox isoform as a potential target for future therapies for atherosclerosis. Reactive Oxygen Species 92-95 cytochrome b-245, beta polypeptide Mus musculus 61-65 19866338-13 2010 In conclusion, the gp91phox-containing NADPH oxidase complex is involved in the central nervous ROS formation after peripheral LPS stimulation and might be a pharmacological target in patients with septic shock. Reactive Oxygen Species 96-99 cytochrome b-245, beta polypeptide Mus musculus 19-27 20500986-7 2010 While several studies on transgenic over-expressing or knockout mice support roles for Nox1- and/or Nox2-containing oxidases as sources of excessive vascular ROS production and causes of endothelial dysfunction in hypertension, atherosclerosis and diabetes, there are still no published reports on the effects of genetic modification of Nox4 or Nox5 in vascular or indeed any other contexts. Reactive Oxygen Species 158-161 cytochrome b-245, beta polypeptide Mus musculus 100-104 19380816-5 2009 The increased ROS production by MDSC is mediated by up-regulated activity of NADPH oxidase (NOX2). Reactive Oxygen Species 14-17 cytochrome b-245, beta polypeptide Mus musculus 92-96 19679834-12 2009 siRNA against the redox-sensitive phosphatase SHP-2 restored EPO-mediated STAT5 induction and inhibition of SHP-2 restored EPO-induced migration in Nox2-deficient cells CONCLUSIONS: We conclude that Nox2-derived ROS inactivate SHP-2 and thereby facilitate EPO signaling in EPCs to promote hypoxia-induced mobilization and vascular repair by these cells. Reactive Oxygen Species 212-215 cytochrome b-245, beta polypeptide Mus musculus 199-203 19409483-4 2009 BMM cells from Nox1 knockout (Nox1(-/-)) as well as Nox2(-/-) mice generated ROS in response to RANKL and differentiated into osteoclasts in the same way as wild-type BMM cells, which was assessed by the appearance of tartrate-resistant acid phosphatase-positive, multinucleated cells having the ability to form resorption pits and by the expression of osteoclast marker genes. Reactive Oxygen Species 77-80 cytochrome b-245, beta polypeptide Mus musculus 52-56 19409483-5 2009 A small interfering RNA (siRNA) targeting Nox1 or Nox2 failed to inhibit the RANKL-stimulated ROS generation and osteoclast formation in wild-type cells, whereas Nox1 and Nox2 siRNAs significantly suppressed the ROS generation and osteoclast formation in Nox2(-/-) and Nox1(-/-) cells, respectively. Reactive Oxygen Species 212-215 cytochrome b-245, beta polypeptide Mus musculus 171-175 19409483-5 2009 A small interfering RNA (siRNA) targeting Nox1 or Nox2 failed to inhibit the RANKL-stimulated ROS generation and osteoclast formation in wild-type cells, whereas Nox1 and Nox2 siRNAs significantly suppressed the ROS generation and osteoclast formation in Nox2(-/-) and Nox1(-/-) cells, respectively. Reactive Oxygen Species 212-215 cytochrome b-245, beta polypeptide Mus musculus 171-175 19409483-7 2009 Collectively, our results suggest that there may be a flexible compensatory mechanism between Nox1 and Nox2 for RANKL-stimulated ROS generation to facilitate osteoclast differentiation. Reactive Oxygen Species 129-132 cytochrome b-245, beta polypeptide Mus musculus 103-107 19679834-3 2009 OBJECTIVE: We studied the contribution of the NADPH oxidase Nox2, an important vascular source of ROS in this context. Reactive Oxygen Species 98-101 cytochrome b-245, beta polypeptide Mus musculus 60-64 19696433-4 2009 ATP-mediated ROS production was strongly attenuated in NOX2-deficient macrophages where responses were comparable to inhibition with diphenyleneiodonium. Reactive Oxygen Species 13-16 cytochrome b-245, beta polypeptide Mus musculus 55-59 19244529-6 2009 In mice lacking the NADPH oxidase subunit NOX2, the ROS increase was not observed, but the CBF increase was still present. Reactive Oxygen Species 52-55 cytochrome b-245, beta polypeptide Mus musculus 42-46 19211495-0 2009 Gender influences cerebral vascular responses to angiotensin II through Nox2-derived reactive oxygen species. Reactive Oxygen Species 85-108 cytochrome b-245, beta polypeptide Mus musculus 72-76 19244529-11 2009 The findings establish a NOX2-containing NADPH oxidase as a major source of ROS produced by NMDA receptor activation, and identify NO as the critical link between NMDA receptor activity and NOX2-dependent ROS production. Reactive Oxygen Species 76-79 cytochrome b-245, beta polypeptide Mus musculus 25-29 19244529-11 2009 The findings establish a NOX2-containing NADPH oxidase as a major source of ROS produced by NMDA receptor activation, and identify NO as the critical link between NMDA receptor activity and NOX2-dependent ROS production. Reactive Oxygen Species 76-79 cytochrome b-245, beta polypeptide Mus musculus 190-194 19244529-11 2009 The findings establish a NOX2-containing NADPH oxidase as a major source of ROS produced by NMDA receptor activation, and identify NO as the critical link between NMDA receptor activity and NOX2-dependent ROS production. Reactive Oxygen Species 205-208 cytochrome b-245, beta polypeptide Mus musculus 25-29 19244529-11 2009 The findings establish a NOX2-containing NADPH oxidase as a major source of ROS produced by NMDA receptor activation, and identify NO as the critical link between NMDA receptor activity and NOX2-dependent ROS production. Reactive Oxygen Species 205-208 cytochrome b-245, beta polypeptide Mus musculus 190-194 18571099-2 2008 The ROS-generating enzyme NADPH oxidase (Nox2) is present in inflammatory cells and contributes to brain injury in adult animal models. Reactive Oxygen Species 4-7 cytochrome b-245, beta polypeptide Mus musculus 41-45 19175604-1 2009 BACKGROUND AND PURPOSE: Reactive oxygen species (ROS) derived from Nox2-containing reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity is reportedly detrimental in cerebrovascular disease. Reactive Oxygen Species 24-47 cytochrome b-245, beta polypeptide Mus musculus 67-71 19175604-1 2009 BACKGROUND AND PURPOSE: Reactive oxygen species (ROS) derived from Nox2-containing reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity is reportedly detrimental in cerebrovascular disease. Reactive Oxygen Species 49-52 cytochrome b-245, beta polypeptide Mus musculus 67-71 18952886-6 2009 Cocaine-induced reactive oxygen species (ROS) production was associated with significant increases ( approximately 2-fold) in the protein expressions of Nox2 (an isoform of NADPH oxidase) and its regulatory subunits: p22(phox), p67(phox), p47(phox), p40(phox), and Rac1, and in p47(phox) phosphorylation as detected by immunoblotting (all p < 0.03). Reactive Oxygen Species 16-39 cytochrome b-245, beta polypeptide Mus musculus 153-157 18952886-6 2009 Cocaine-induced reactive oxygen species (ROS) production was associated with significant increases ( approximately 2-fold) in the protein expressions of Nox2 (an isoform of NADPH oxidase) and its regulatory subunits: p22(phox), p67(phox), p47(phox), p40(phox), and Rac1, and in p47(phox) phosphorylation as detected by immunoblotting (all p < 0.03). Reactive Oxygen Species 41-44 cytochrome b-245, beta polypeptide Mus musculus 153-157 19005069-2 2008 Microglia, the resident CNS macrophages, are prominent sources of ROS through expression of the phagocyte oxidase which catalytic subunit Nox2 generates superoxide ion (O2(.-)). Reactive Oxygen Species 66-69 cytochrome b-245, beta polypeptide Mus musculus 138-142 18583711-9 2008 In conclusion, Nox2-derived ROS in BM play a critical role in mobilization, homing, and angiogenic capacity of EPCs and BM stem/progenitor cells, thereby promoting revascularization of ischemic tissue. Reactive Oxygen Species 28-31 cytochrome b-245, beta polypeptide Mus musculus 15-19 19096031-0 2009 Macrophages generate reactive oxygen species in response to minimally oxidized low-density lipoprotein: toll-like receptor 4- and spleen tyrosine kinase-dependent activation of NADPH oxidase 2. Reactive Oxygen Species 21-44 cytochrome b-245, beta polypeptide Mus musculus 177-192 19096031-2 2009 In this study, we demonstrate that minimally oxidized LDL (mmLDL) stimulates intracellular reactive oxygen species (ROS) generation in macrophages through NADPH oxidase 2 (gp91phox/Nox2), which, in turn, induces production of RANTES and migration of smooth muscle cells. Reactive Oxygen Species 91-114 cytochrome b-245, beta polypeptide Mus musculus 155-170 19096031-2 2009 In this study, we demonstrate that minimally oxidized LDL (mmLDL) stimulates intracellular reactive oxygen species (ROS) generation in macrophages through NADPH oxidase 2 (gp91phox/Nox2), which, in turn, induces production of RANTES and migration of smooth muscle cells. Reactive Oxygen Species 91-114 cytochrome b-245, beta polypeptide Mus musculus 172-180 19096031-2 2009 In this study, we demonstrate that minimally oxidized LDL (mmLDL) stimulates intracellular reactive oxygen species (ROS) generation in macrophages through NADPH oxidase 2 (gp91phox/Nox2), which, in turn, induces production of RANTES and migration of smooth muscle cells. Reactive Oxygen Species 91-114 cytochrome b-245, beta polypeptide Mus musculus 181-185 19096031-2 2009 In this study, we demonstrate that minimally oxidized LDL (mmLDL) stimulates intracellular reactive oxygen species (ROS) generation in macrophages through NADPH oxidase 2 (gp91phox/Nox2), which, in turn, induces production of RANTES and migration of smooth muscle cells. Reactive Oxygen Species 116-119 cytochrome b-245, beta polypeptide Mus musculus 155-170 19096031-2 2009 In this study, we demonstrate that minimally oxidized LDL (mmLDL) stimulates intracellular reactive oxygen species (ROS) generation in macrophages through NADPH oxidase 2 (gp91phox/Nox2), which, in turn, induces production of RANTES and migration of smooth muscle cells. Reactive Oxygen Species 116-119 cytochrome b-245, beta polypeptide Mus musculus 172-180 19096031-2 2009 In this study, we demonstrate that minimally oxidized LDL (mmLDL) stimulates intracellular reactive oxygen species (ROS) generation in macrophages through NADPH oxidase 2 (gp91phox/Nox2), which, in turn, induces production of RANTES and migration of smooth muscle cells. Reactive Oxygen Species 116-119 cytochrome b-245, beta polypeptide Mus musculus 181-185 19096031-9 2009 These results suggest that mmLDL induces generation of ROS through sequential activation of TLR4, Syk, phospholipase Cgamma1, protein kinase C, and gp91phox/Nox2 and thereby stimulates expression of proinflammatory cytokines. Reactive Oxygen Species 55-58 cytochrome b-245, beta polypeptide Mus musculus 148-156 19096031-9 2009 These results suggest that mmLDL induces generation of ROS through sequential activation of TLR4, Syk, phospholipase Cgamma1, protein kinase C, and gp91phox/Nox2 and thereby stimulates expression of proinflammatory cytokines. Reactive Oxygen Species 55-58 cytochrome b-245, beta polypeptide Mus musculus 157-161 18987286-15 2009 NOX2-derived ROS scavenges nitric oxide, causing subsequent nitric oxide-deficiency. Reactive Oxygen Species 13-16 cytochrome b-245, beta polypeptide Mus musculus 0-4 18573285-5 2008 The subsequent response was increased ROS production associated with activation of NADPH oxidase (NOX2) and then phosphorylation of MAP kinases (Erk, JNK). Reactive Oxygen Species 38-41 cytochrome b-245, beta polypeptide Mus musculus 98-102 18583711-3 2008 Reactive oxygen species (ROS) derived from Nox2-based NADPH oxidase play an important role in postnatal neovascularization; however, their role in BM and EPC function is unknown. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 43-47 18583711-3 2008 Reactive oxygen species (ROS) derived from Nox2-based NADPH oxidase play an important role in postnatal neovascularization; however, their role in BM and EPC function is unknown. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 43-47 18583711-5 2008 Mice lacking Nox2 show reduction of ischemia-induced flow recovery, ROS levels in BMCs, as well as EPC mobilization from BM. Reactive Oxygen Species 68-71 cytochrome b-245, beta polypeptide Mus musculus 13-17 18571099-12 2008 CONCLUSION: NADPH oxidase is upregulated after hypoxia-ischemia and activated microglia cells are a possible source of Nox2-derived ROS. Reactive Oxygen Species 132-135 cytochrome b-245, beta polypeptide Mus musculus 119-123 16894058-3 2006 We investigated whether a Nox2-containing NADPH oxidase is the source of the Ang II-induced ROS production and whether the signaling mechanisms of its activation require intracellular Ca(2+) or protein kinase C (PKC). Reactive Oxygen Species 92-95 cytochrome b-245, beta polypeptide Mus musculus 26-30 17916764-13 2007 CONCLUSIONS: Activation of Rac and subsequently of the gp91phox containing NADPH oxidase promotes cerebral ROS formation, which then leads to Rho kinase-mediated endothelial cell contraction and disruption of the BBB. Reactive Oxygen Species 107-110 cytochrome b-245, beta polypeptide Mus musculus 55-63 17138940-1 2007 OBJECTIVE: Angiotensin II (AngII) disrupts the regulation of the cerebral circulation through superoxide, a reactive oxygen species (ROS) generated by a nox2-containing NADPH oxidase. Reactive Oxygen Species 108-131 cytochrome b-245, beta polypeptide Mus musculus 153-157 17138940-1 2007 OBJECTIVE: Angiotensin II (AngII) disrupts the regulation of the cerebral circulation through superoxide, a reactive oxygen species (ROS) generated by a nox2-containing NADPH oxidase. Reactive Oxygen Species 133-136 cytochrome b-245, beta polypeptide Mus musculus 153-157 17138940-5 2007 AngII also increased the nitration marker 3-nitrotyrosine (3-NT) in cerebral blood vessels, an effect dependent on NO and nox2-derived ROS. Reactive Oxygen Species 135-138 cytochrome b-245, beta polypeptide Mus musculus 122-126 17429347-0 2007 Nox2-derived reactive oxygen species mediate neurovascular dysregulation in the aging mouse brain. Reactive Oxygen Species 13-36 cytochrome b-245, beta polypeptide Mus musculus 0-4 17429347-8 2007 The cerebrovascular impairment present in 12-month-old mice was reversed by the ROS scavenger Mn (III) tetrakis (4-benzoic acid) porphyrin chloride or by the NADPH oxidase peptide inhibitor gp91ds-tat, and was not observed in mice lacking the Nox2 subunit of NADPH oxidase. Reactive Oxygen Species 80-83 cytochrome b-245, beta polypeptide Mus musculus 243-247 17363703-9 2007 Increased ROS production from endothelial Nox2 overexpression led to increased endothelial nitric oxide synthase protein and extracellular signal-regulated kinase 1/2 phosphorylation in transgenic aortas. Reactive Oxygen Species 10-13 cytochrome b-245, beta polypeptide Mus musculus 42-46 16820798-7 2007 In contrast, ROS production and brain injury were reduced in mice lacking the nox2 subunit of the superoxide-producing enzyme nicotinamide adenine dinucleotide phosphate (reduced form) oxidase. Reactive Oxygen Species 13-16 cytochrome b-245, beta polypeptide Mus musculus 78-82 17365667-8 2007 ROS increase during H/RA was prevented by deletion of gp91phox or p47phox, or MAPK inhibition. Reactive Oxygen Species 0-3 cytochrome b-245, beta polypeptide Mus musculus 54-62 16894058-10 2006 We conclude that the powerful effects of Ang II on Ca(2+) currents in dmNTS neurons are mediated by PKC activation leading to ROS production via Nox2. Reactive Oxygen Species 126-129 cytochrome b-245, beta polypeptide Mus musculus 145-149 16439707-8 2006 The source of the ROS is a nox-2-containing NADPH oxidase. Reactive Oxygen Species 18-21 cytochrome b-245, beta polypeptide Mus musculus 27-32 16715116-18 2006 In extrapulmonary arteries from hypoxic mice, endothelium-dependent relaxation appears to be mediated by ROS, in a gp91phox-independent manner. Reactive Oxygen Species 105-108 cytochrome b-245, beta polypeptide Mus musculus 115-123 16109921-9 2005 In both control and gp91phox(-/-) animals, reactive oxygen species (ROS) production and MMP induction was enhanced by AVF, whereas in p47phox(-/-) and eNOS(-/-) mice such response was negligible. Reactive Oxygen Species 43-66 cytochrome b-245, beta polypeptide Mus musculus 20-28 16085672-5 2006 The CH-induced increase in the generation of ROS was obliterated in NADPH oxidase (gp91phox) knockout (KO) mice, suggesting that NADPH oxidase was the major source of ROS. Reactive Oxygen Species 45-48 cytochrome b-245, beta polypeptide Mus musculus 83-91 16085672-5 2006 The CH-induced increase in the generation of ROS was obliterated in NADPH oxidase (gp91phox) knockout (KO) mice, suggesting that NADPH oxidase was the major source of ROS. Reactive Oxygen Species 167-170 cytochrome b-245, beta polypeptide Mus musculus 83-91 16321801-7 2005 The Abeta induced increase in ROS and the mitochondrial depolarization were absent in cells cultured from transgenic mice lacking the NOX component, gp91phox. Reactive Oxygen Species 30-33 cytochrome b-245, beta polypeptide Mus musculus 149-157 16236999-2 2005 A NOX-2-containing NADPH oxidase is a recognized major source of ROS in cardiac myocytes, whose activity is augmented by preconditioning mimetics, such as angiotensin II. Reactive Oxygen Species 65-68 cytochrome b-245, beta polypeptide Mus musculus 2-7 15753233-1 2005 The gp91phox-containing NADPH oxidase is the major source of reactive oxygen species (ROS) in the cardiovascular system and inactivation of gp91phox has been reported to blunt hypertension and cardiac hypertrophy seen in angiotensin (Ang) II-infused animals. Reactive Oxygen Species 61-84 cytochrome b-245, beta polypeptide Mus musculus 4-12 15867174-2 2005 We reported that reactive oxygen species (ROS) derived from gp91phox (Nox2)-containing NAD(P)H oxidase are involved in angiogenesis in mouse sponge models as well as in vascular endothelial growth factor (VEGF) signaling in cultured endothelial cells. Reactive Oxygen Species 17-40 cytochrome b-245, beta polypeptide Mus musculus 60-68 15867174-2 2005 We reported that reactive oxygen species (ROS) derived from gp91phox (Nox2)-containing NAD(P)H oxidase are involved in angiogenesis in mouse sponge models as well as in vascular endothelial growth factor (VEGF) signaling in cultured endothelial cells. Reactive Oxygen Species 17-40 cytochrome b-245, beta polypeptide Mus musculus 70-74 15867174-2 2005 We reported that reactive oxygen species (ROS) derived from gp91phox (Nox2)-containing NAD(P)H oxidase are involved in angiogenesis in mouse sponge models as well as in vascular endothelial growth factor (VEGF) signaling in cultured endothelial cells. Reactive Oxygen Species 42-45 cytochrome b-245, beta polypeptide Mus musculus 60-68 15867174-2 2005 We reported that reactive oxygen species (ROS) derived from gp91phox (Nox2)-containing NAD(P)H oxidase are involved in angiogenesis in mouse sponge models as well as in vascular endothelial growth factor (VEGF) signaling in cultured endothelial cells. Reactive Oxygen Species 42-45 cytochrome b-245, beta polypeptide Mus musculus 70-74 15867174-8 2005 Relative to WT mice, ischemia-induced ROS production in gp91phox-/- mice at both 3 and 7 days was diminished, whereas VEGF expression was enhanced and the inflammatory response was unchanged. Reactive Oxygen Species 38-41 cytochrome b-245, beta polypeptide Mus musculus 56-64 15867174-10 2005 CONCLUSIONS: gp91phox-derived ROS play an important role in mediating neovascularization in response to tissue ischemia. Reactive Oxygen Species 30-33 cytochrome b-245, beta polypeptide Mus musculus 13-21 15753233-1 2005 The gp91phox-containing NADPH oxidase is the major source of reactive oxygen species (ROS) in the cardiovascular system and inactivation of gp91phox has been reported to blunt hypertension and cardiac hypertrophy seen in angiotensin (Ang) II-infused animals. Reactive Oxygen Species 61-84 cytochrome b-245, beta polypeptide Mus musculus 140-148 15753233-1 2005 The gp91phox-containing NADPH oxidase is the major source of reactive oxygen species (ROS) in the cardiovascular system and inactivation of gp91phox has been reported to blunt hypertension and cardiac hypertrophy seen in angiotensin (Ang) II-infused animals. Reactive Oxygen Species 86-89 cytochrome b-245, beta polypeptide Mus musculus 4-12 15753233-11 2005 Thus, although eliminating gp91phox-associated ROS production may be important in cardiovascular consequences in acute insult models, it does not prevent the development of hypertension and cardiac hypertrophy in a model in which the endogenous renin-angiotensin system is chronically upregulated. Reactive Oxygen Species 47-50 cytochrome b-245, beta polypeptide Mus musculus 27-35 15499027-10 2004 Collectively, these findings suggest that Ang II impairs functional hyperemia by activating AT1 receptors and inducing ROS production via a gp91phox containing NADPH oxidase. Reactive Oxygen Species 119-122 cytochrome b-245, beta polypeptide Mus musculus 140-148 12855428-7 2003 Consistent with the observations in situ, basal and stimulated ROS levels were reduced in FB isolated from aorta of gp91phox KO compared with FB from wild-type aorta, whereas ROS levels were similar in SMC derived from gp91phox KO and wild-type aorta. Reactive Oxygen Species 63-66 cytochrome b-245, beta polypeptide Mus musculus 116-124 12855428-12 2003 Confirming functional expression of gp91phox in FB, antisense to gp91phox decreased ROS levels in wild-type FB. Reactive Oxygen Species 84-87 cytochrome b-245, beta polypeptide Mus musculus 36-44 12855428-12 2003 Confirming functional expression of gp91phox in FB, antisense to gp91phox decreased ROS levels in wild-type FB. Reactive Oxygen Species 84-87 cytochrome b-245, beta polypeptide Mus musculus 65-73 10884368-0 2000 A gp91phox containing NADPH oxidase selectively expressed in endothelial cells is a major source of oxygen radical generation in the arterial wall. Reactive Oxygen Species 100-114 cytochrome b-245, beta polypeptide Mus musculus 2-10 14551238-2 2003 Phagocyte-type NADPH oxidases are major cardiovascular sources of ROS, and recent data indicate a pivotal role of a gp91phox-containing NADPH oxidase in angiotensin II (Ang II)-induced LVH. Reactive Oxygen Species 66-69 cytochrome b-245, beta polypeptide Mus musculus 116-124 12967772-5 2003 Studies in mice that are deficient in p47(phox) and gp91(phox) (also known as NOX2) NAD(P)H oxidase subunits show that ROS produced by these oxidases contribute to cardiovascular diseases including atherosclerosis and hypertension. Reactive Oxygen Species 119-122 cytochrome b-245, beta polypeptide Mus musculus 78-82 10884368-9 2000 PMA-induced ROS generation was comparable in aortae from wild-type and eNOS(-/-) mice, but was attenuated in segments from gp91phox(-/-) mice. Reactive Oxygen Species 12-15 cytochrome b-245, beta polypeptide Mus musculus 123-131 33237428-0 2020 Hyperglycemia regulates cardiac K+ channels via O-GlcNAc-CaMKII and NOX2-ROS-PKC pathways. Reactive Oxygen Species 73-76 cytochrome b-245, beta polypeptide Mus musculus 68-72 33237428-6 2020 Ito reduction was prevented by inhibition of protein kinase C (PKC) and NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS). Reactive Oxygen Species 103-126 cytochrome b-245, beta polypeptide Mus musculus 72-87 33237428-6 2020 Ito reduction was prevented by inhibition of protein kinase C (PKC) and NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS). Reactive Oxygen Species 103-126 cytochrome b-245, beta polypeptide Mus musculus 89-93 33237428-6 2020 Ito reduction was prevented by inhibition of protein kinase C (PKC) and NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS). Reactive Oxygen Species 128-131 cytochrome b-245, beta polypeptide Mus musculus 72-87 33237428-6 2020 Ito reduction was prevented by inhibition of protein kinase C (PKC) and NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS). Reactive Oxygen Species 128-131 cytochrome b-245, beta polypeptide Mus musculus 89-93 33237428-9 2020 We conclude that acute hyperglycemia enhances IK1 and Ito recovery via CaMKIIdelta-S280 O-GlcNAcylation, but reduces Ito amplitude via a NOX2-ROS-PKC pathway. Reactive Oxygen Species 142-145 cytochrome b-245, beta polypeptide Mus musculus 137-141 29277898-8 2018 G6PD inhibitor led to reduction of LPS-induced airway inflammation, bronchoalveolar lavage fluid protein concentration as well as NOX2-derived ROS and subsequent oxidative stress. Reactive Oxygen Species 143-146 cytochrome b-245, beta polypeptide Mus musculus 130-134 34920732-2 2021 The production of excess reactive oxygen species (ROS) mediated by nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) and the maturation of inflammatory cytokines caused by activation of the NOD-like receptor protein 1 (NLRP1) inflammasome play central roles in promoting brain aging. Reactive Oxygen Species 25-48 cytochrome b-245, beta polypeptide Mus musculus 67-120 29277898-3 2018 Reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) are thought to play an important role in the pathophysiology of ALI. Reactive Oxygen Species 0-23 cytochrome b-245, beta polypeptide Mus musculus 104-108 29277898-3 2018 Reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) are thought to play an important role in the pathophysiology of ALI. Reactive Oxygen Species 25-28 cytochrome b-245, beta polypeptide Mus musculus 104-108 29277898-5 2018 However, how G6PD modulation affects NOX2-mediated ROS in the airway epithelial cells (AECs) during acute lung injury has not been explored previously. Reactive Oxygen Species 51-54 cytochrome b-245, beta polypeptide Mus musculus 37-41 34920732-2 2021 The production of excess reactive oxygen species (ROS) mediated by nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) and the maturation of inflammatory cytokines caused by activation of the NOD-like receptor protein 1 (NLRP1) inflammasome play central roles in promoting brain aging. Reactive Oxygen Species 50-53 cytochrome b-245, beta polypeptide Mus musculus 67-120 34509916-11 2021 Effects of IL-6 on activating NOX2-dependent ROS production and upregulation of MCP-1 were also completely attenuated by 17beta-estradiol. Reactive Oxygen Species 45-48 cytochrome b-245, beta polypeptide Mus musculus 30-34 34755642-7 2022 Concomitantly, AngII induced an increase in ROS production that was sensitive to the NOX2 specific inhibitor gp91ds-tat (1 mumol/L). Reactive Oxygen Species 44-47 cytochrome b-245, beta polypeptide Mus musculus 85-89 34755642-10 2022 AngII induced IICR in Nox2-/- AMs could be restored by addition of exogenous ROS (tert-butyl hydroperoxide, tBHP: 5 mumol/L). Reactive Oxygen Species 77-80 cytochrome b-245, beta polypeptide Mus musculus 22-26 34755642-14 2022 Our data demonstrate that in AMs the InsP3R is under dual control of agonist induced InsP3 and ROS formation and suggest that InsP3 and NOX2-derived ROS co-regulate atrial IICR and ECC in a defined InsP3R/NOX2 signaling domain. Reactive Oxygen Species 149-152 cytochrome b-245, beta polypeptide Mus musculus 136-140 34755642-14 2022 Our data demonstrate that in AMs the InsP3R is under dual control of agonist induced InsP3 and ROS formation and suggest that InsP3 and NOX2-derived ROS co-regulate atrial IICR and ECC in a defined InsP3R/NOX2 signaling domain. Reactive Oxygen Species 149-152 cytochrome b-245, beta polypeptide Mus musculus 205-209 34829547-3 2021 We used the cecal ligation and puncture (CLP) model of ALI associated with sepsis to investigate the effect of inhibiting NADPH oxidase 2 (NOX2)-derived ROS production, the main source of ROS in lungs. Reactive Oxygen Species 153-156 cytochrome b-245, beta polypeptide Mus musculus 122-137 34829547-3 2021 We used the cecal ligation and puncture (CLP) model of ALI associated with sepsis to investigate the effect of inhibiting NADPH oxidase 2 (NOX2)-derived ROS production, the main source of ROS in lungs. Reactive Oxygen Species 153-156 cytochrome b-245, beta polypeptide Mus musculus 139-143 34829547-3 2021 We used the cecal ligation and puncture (CLP) model of ALI associated with sepsis to investigate the effect of inhibiting NADPH oxidase 2 (NOX2)-derived ROS production, the main source of ROS in lungs. Reactive Oxygen Species 188-191 cytochrome b-245, beta polypeptide Mus musculus 122-137 34829547-3 2021 We used the cecal ligation and puncture (CLP) model of ALI associated with sepsis to investigate the effect of inhibiting NADPH oxidase 2 (NOX2)-derived ROS production, the main source of ROS in lungs. Reactive Oxygen Species 188-191 cytochrome b-245, beta polypeptide Mus musculus 139-143 34829531-6 2021 Mice were either fed a standard diet or Western diet (WD) to study a possible interaction between NOX2-derived ROS and LDL. Reactive Oxygen Species 111-114 cytochrome b-245, beta polypeptide Mus musculus 98-102 34829531-9 2021 Nox2-/- macrophages produced basal levels of ROS but were unable to increase ROS production in response to the alarmin S100A8 or the phorbol ester PMA. Reactive Oxygen Species 45-48 cytochrome b-245, beta polypeptide Mus musculus 0-4 34829531-11 2021 These results suggest that NOX2-derived ROS are involved in CiOA development. Reactive Oxygen Species 40-43 cytochrome b-245, beta polypeptide Mus musculus 27-31 34666785-7 2021 The underlying mechanism for negative effects of LPAR1-3 antagonist was associated with the overproduction of reactive oxygen species (ROS)-generating nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) 2 and NOX3. Reactive Oxygen Species 110-133 cytochrome b-245, beta polypeptide Mus musculus 151-219 34666785-7 2021 The underlying mechanism for negative effects of LPAR1-3 antagonist was associated with the overproduction of reactive oxygen species (ROS)-generating nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) 2 and NOX3. Reactive Oxygen Species 135-138 cytochrome b-245, beta polypeptide Mus musculus 151-219 34116239-2 2021 We sought to determine if NADPH oxidase 2 (NOX2)-derived ROS underpin CIH-induced maladaptive changes in respiratory control. Reactive Oxygen Species 57-60 cytochrome b-245, beta polypeptide Mus musculus 26-41 34116239-2 2021 We sought to determine if NADPH oxidase 2 (NOX2)-derived ROS underpin CIH-induced maladaptive changes in respiratory control. Reactive Oxygen Species 57-60 cytochrome b-245, beta polypeptide Mus musculus 43-47 34557202-11 2021 Our results suggest that NOX2-derived ROS is critical for regulating the function and gene expression in arthritic neutrophils. Reactive Oxygen Species 38-41 cytochrome b-245, beta polypeptide Mus musculus 25-29 34439486-10 2021 These findings provide evidence that Ang II induces endothelial dysfunction in mouse ophthalmic arteries via AT1R activation and NOX2-dependent ROS formation. Reactive Oxygen Species 144-147 cytochrome b-245, beta polypeptide Mus musculus 129-133 34572995-1 2021 The p47phox is a key regulatory subunit of Nox2-containing NADPH oxidase (Nox2) that by generating reactive oxygen species (ROS) plays an important role in Angiotensin II (AngII)-induced cardiac hypertrophy and heart failure. Reactive Oxygen Species 99-122 cytochrome b-245, beta polypeptide Mus musculus 43-47 34572995-1 2021 The p47phox is a key regulatory subunit of Nox2-containing NADPH oxidase (Nox2) that by generating reactive oxygen species (ROS) plays an important role in Angiotensin II (AngII)-induced cardiac hypertrophy and heart failure. Reactive Oxygen Species 99-122 cytochrome b-245, beta polypeptide Mus musculus 74-78 34572995-1 2021 The p47phox is a key regulatory subunit of Nox2-containing NADPH oxidase (Nox2) that by generating reactive oxygen species (ROS) plays an important role in Angiotensin II (AngII)-induced cardiac hypertrophy and heart failure. Reactive Oxygen Species 124-127 cytochrome b-245, beta polypeptide Mus musculus 43-47 34572995-1 2021 The p47phox is a key regulatory subunit of Nox2-containing NADPH oxidase (Nox2) that by generating reactive oxygen species (ROS) plays an important role in Angiotensin II (AngII)-induced cardiac hypertrophy and heart failure. Reactive Oxygen Species 124-127 cytochrome b-245, beta polypeptide Mus musculus 74-78 34174253-6 2021 Immunohistochemical studies revealed that the salivary gland lesions strongly expressed four sialadenitis-related molecules: SSA and SSB (autoantigens of Sjogren"s syndrome), gp91phox (an accelerator of reactive oxygen species production) and single strand DNA (a marker of apoptotic cells). Reactive Oxygen Species 203-226 cytochrome b-245, beta polypeptide Mus musculus 175-183 34439552-10 2021 As early NOX2-driven ROS production impacts beta-cells" function and survival during insulitis, NOX2 might be a potential target for designing therapies against early beta-cell dysfunction in the context of T1D onset. Reactive Oxygen Species 21-24 cytochrome b-245, beta polypeptide Mus musculus 9-13 34099836-1 2021 The NADPH oxidase enzymes Nox2 and 4, are important generators of Reactive oxygen species (ROS). Reactive Oxygen Species 66-89 cytochrome b-245, beta polypeptide Mus musculus 26-36 34134732-12 2021 Moreover, selective inhibition of NADPH oxidase 2 (NOX2) was sufficient to inhibit endosomal ROS bursts and induction of chemokine expressions in cells treated with silica NPs, suggesting the central role of endosomal ROS generated by NOX2 in the regulation of the inflammatory response in macrophages that endocytosed silica NPs. Reactive Oxygen Species 93-96 cytochrome b-245, beta polypeptide Mus musculus 34-49 34134732-12 2021 Moreover, selective inhibition of NADPH oxidase 2 (NOX2) was sufficient to inhibit endosomal ROS bursts and induction of chemokine expressions in cells treated with silica NPs, suggesting the central role of endosomal ROS generated by NOX2 in the regulation of the inflammatory response in macrophages that endocytosed silica NPs. Reactive Oxygen Species 93-96 cytochrome b-245, beta polypeptide Mus musculus 51-55 34134732-12 2021 Moreover, selective inhibition of NADPH oxidase 2 (NOX2) was sufficient to inhibit endosomal ROS bursts and induction of chemokine expressions in cells treated with silica NPs, suggesting the central role of endosomal ROS generated by NOX2 in the regulation of the inflammatory response in macrophages that endocytosed silica NPs. Reactive Oxygen Species 93-96 cytochrome b-245, beta polypeptide Mus musculus 235-239 34134732-12 2021 Moreover, selective inhibition of NADPH oxidase 2 (NOX2) was sufficient to inhibit endosomal ROS bursts and induction of chemokine expressions in cells treated with silica NPs, suggesting the central role of endosomal ROS generated by NOX2 in the regulation of the inflammatory response in macrophages that endocytosed silica NPs. Reactive Oxygen Species 218-221 cytochrome b-245, beta polypeptide Mus musculus 34-49 34134732-12 2021 Moreover, selective inhibition of NADPH oxidase 2 (NOX2) was sufficient to inhibit endosomal ROS bursts and induction of chemokine expressions in cells treated with silica NPs, suggesting the central role of endosomal ROS generated by NOX2 in the regulation of the inflammatory response in macrophages that endocytosed silica NPs. Reactive Oxygen Species 218-221 cytochrome b-245, beta polypeptide Mus musculus 51-55 34134732-12 2021 Moreover, selective inhibition of NADPH oxidase 2 (NOX2) was sufficient to inhibit endosomal ROS bursts and induction of chemokine expressions in cells treated with silica NPs, suggesting the central role of endosomal ROS generated by NOX2 in the regulation of the inflammatory response in macrophages that endocytosed silica NPs. Reactive Oxygen Species 218-221 cytochrome b-245, beta polypeptide Mus musculus 235-239 34134732-14 2021 Cellular uptake of larger particles by macrophages decreased, while surface amine modification modulated endosomal ROS signaling via NOX2, both of which are assumed to be involved in mitigating immune response in macrophages and resulting lung injury. Reactive Oxygen Species 115-118 cytochrome b-245, beta polypeptide Mus musculus 133-137 34394834-7 2021 Furthermore, the shHamp mice showed a decrease of ROS by downregulating the elevated NADPH oxidase (NOX2) and 4-hydroxynonenal (4-HNE) levels mediated by CIH. Reactive Oxygen Species 50-53 cytochrome b-245, beta polypeptide Mus musculus 100-104 34099836-1 2021 The NADPH oxidase enzymes Nox2 and 4, are important generators of Reactive oxygen species (ROS). Reactive Oxygen Species 91-94 cytochrome b-245, beta polypeptide Mus musculus 26-36 34099836-6 2021 We conclude that a pharmacological and partial inhibition of ROS production by inhibition of Nox 2 and 4 is beneficial for recovery after ischemia reperfusion and might be a promising venue for treatment of ischemic injury to the heart. Reactive Oxygen Species 61-64 cytochrome b-245, beta polypeptide Mus musculus 93-104 35008006-5 2022 Mechanistically, CTRP9 increased the levels of NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS). Reactive Oxygen Species 78-101 cytochrome b-245, beta polypeptide Mus musculus 47-62 35430393-0 2022 Novel potential NOX2 inhibitors, Dudleya brittonii water extract and polygalatenoside A inhibit intracellular ROS generation and growth of melanoma. Reactive Oxygen Species 110-113 cytochrome b-245, beta polypeptide Mus musculus 16-20 35430393-3 2022 This study showed altered NADPH oxidase 2 (NOX2) expression and selective inhibition of cytosolic ROS but not mitochondrial ROS in B16-F10 melanoma cells, suggesting the NOX2 inhibitory potential of DBWE. Reactive Oxygen Species 98-101 cytochrome b-245, beta polypeptide Mus musculus 170-174 35597360-9 2022 Conversely, inhibition of the TLR4/NOX2 signalling pathway effectively reduced the level of ROS in cells, weakened the upregulation of Notch and TGF-beta signalling by PS-MPs, and efficiently reduced the expression of fibrotic and collagen genes. Reactive Oxygen Species 92-95 cytochrome b-245, beta polypeptide Mus musculus 35-39 35624895-12 2022 These results demonstrate that the susceptibility of OPCs and mOLs to ultrafine DEPs is, at least in part, caused by excessive ROS produced by NOX2 and the sequential changes in the expression of p53, Bax, Bcl-2, and cleaved caspase-3. Reactive Oxygen Species 127-130 cytochrome b-245, beta polypeptide Mus musculus 143-147 35377790-2 2022 ROS generation in MDSC occurs during the oxidation of NADPH to NADP+, which NOX2 catalyzes. Reactive Oxygen Species 0-3 cytochrome b-245, beta polypeptide Mus musculus 76-80 35008006-5 2022 Mechanistically, CTRP9 increased the levels of NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS). Reactive Oxygen Species 78-101 cytochrome b-245, beta polypeptide Mus musculus 64-68 35008006-5 2022 Mechanistically, CTRP9 increased the levels of NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS). Reactive Oxygen Species 103-106 cytochrome b-245, beta polypeptide Mus musculus 47-62 35008006-5 2022 Mechanistically, CTRP9 increased the levels of NADPH oxidase 2 (NOX2)-derived reactive oxygen species (ROS). Reactive Oxygen Species 103-106 cytochrome b-245, beta polypeptide Mus musculus 64-68 35008006-10 2022 In conclusion, our study indicates that CTRP9 aggravates LPS-induced inflammation by promoting NLRP3 inflammasome activation via the NOX2/ROS pathway. Reactive Oxygen Species 138-141 cytochrome b-245, beta polypeptide Mus musculus 133-137 35057820-6 2022 Mechanistically, AuNPs and LPS coordinate to upregulate NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS) generation and activate the intrinsic apoptotic pathway in hepatic macrophages. Reactive Oxygen Species 89-112 cytochrome b-245, beta polypeptide Mus musculus 56-71 35102790-2 2022 A proposed mediator is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2), a major source of reactive oxygen species (ROS) in the brain. Reactive Oxygen Species 111-134 cytochrome b-245, beta polypeptide Mus musculus 23-84 35102790-2 2022 A proposed mediator is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2), a major source of reactive oxygen species (ROS) in the brain. Reactive Oxygen Species 111-134 cytochrome b-245, beta polypeptide Mus musculus 86-90 35102790-2 2022 A proposed mediator is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2), a major source of reactive oxygen species (ROS) in the brain. Reactive Oxygen Species 136-139 cytochrome b-245, beta polypeptide Mus musculus 23-84 35102790-2 2022 A proposed mediator is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2), a major source of reactive oxygen species (ROS) in the brain. Reactive Oxygen Species 136-139 cytochrome b-245, beta polypeptide Mus musculus 86-90 35057820-6 2022 Mechanistically, AuNPs and LPS coordinate to upregulate NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS) generation and activate the intrinsic apoptotic pathway in hepatic macrophages. Reactive Oxygen Species 89-112 cytochrome b-245, beta polypeptide Mus musculus 73-77 35057820-6 2022 Mechanistically, AuNPs and LPS coordinate to upregulate NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS) generation and activate the intrinsic apoptotic pathway in hepatic macrophages. Reactive Oxygen Species 114-117 cytochrome b-245, beta polypeptide Mus musculus 56-71 35057820-6 2022 Mechanistically, AuNPs and LPS coordinate to upregulate NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS) generation and activate the intrinsic apoptotic pathway in hepatic macrophages. Reactive Oxygen Species 114-117 cytochrome b-245, beta polypeptide Mus musculus 73-77