PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32531347-3 2020 The ROS production by NOX2 involves the assembly of the cytosolic subunits (p67phox, p47phox, and p40phox) and Rac with the membrane subunits (gp91phox and p22phox). Reactive Oxygen Species 4-7 Rac family small GTPase 1 Homo sapiens 111-114 33852856-5 2021 We further identify the Rac1-NADPH oxidase (NOX) complex as the major cause of reactive oxygen species (ROS) accumulation in ifc-knockout (ifc-KO) photoreceptors and in SH-SY5Y cells with the leukodystrophy-associated DEGS1H132R variant. Reactive Oxygen Species 79-102 Rac family small GTPase 1 Homo sapiens 24-28 33852856-5 2021 We further identify the Rac1-NADPH oxidase (NOX) complex as the major cause of reactive oxygen species (ROS) accumulation in ifc-knockout (ifc-KO) photoreceptors and in SH-SY5Y cells with the leukodystrophy-associated DEGS1H132R variant. Reactive Oxygen Species 104-107 Rac family small GTPase 1 Homo sapiens 24-28 32627008-6 2020 We further demonstrated that high mtAPE1 expression could downregulate ROS production by decreasing the phosphorylation of Rac1 (p-Rac1), further promoting cisplatin resistance in osteosarcoma. Reactive Oxygen Species 71-74 Rac family small GTPase 1 Homo sapiens 123-127 30105917-3 2019 In the pathogenesis of diabetic retinopathy, a progressive disease, reactive oxygen species (ROS) production by activation of a small molecular weight G-protein (Ras-related C3 botulinum toxin substrate 1 [Rac1])-Nox2 signaling precedes mitochondrial damage. Reactive Oxygen Species 68-91 Rac family small GTPase 1 Homo sapiens 162-204 32300016-7 2020 Additionally, RvE1-triggered activation of the small GTPase Rac1 led to increased intracellular reactive oxygen species (ROS) production, cell-matrix adhesion, and cellular protrusions at the leading edge of migrating cells. Reactive Oxygen Species 96-119 Rac family small GTPase 1 Homo sapiens 60-64 32300016-7 2020 Additionally, RvE1-triggered activation of the small GTPase Rac1 led to increased intracellular reactive oxygen species (ROS) production, cell-matrix adhesion, and cellular protrusions at the leading edge of migrating cells. Reactive Oxygen Species 121-124 Rac family small GTPase 1 Homo sapiens 60-64 32178475-4 2020 Downstream, Rac1 initiates a series of signaling networks, including regulatory complex of actin cytoskeleton remodeling, activation of protein kinases (PAKs, MAPKs) and transcription factors (NFkB, Wnt/beta-catenin/TCF, STAT3, Snail), production of reactive oxygen species (NADPH oxidase holoenzymes, mitochondrial ROS). Reactive Oxygen Species 250-273 Rac family small GTPase 1 Homo sapiens 12-16 32178475-4 2020 Downstream, Rac1 initiates a series of signaling networks, including regulatory complex of actin cytoskeleton remodeling, activation of protein kinases (PAKs, MAPKs) and transcription factors (NFkB, Wnt/beta-catenin/TCF, STAT3, Snail), production of reactive oxygen species (NADPH oxidase holoenzymes, mitochondrial ROS). Reactive Oxygen Species 316-319 Rac family small GTPase 1 Homo sapiens 12-16 32133799-4 2020 DOX-related reactive oxygen species (ROS) were found to be responsible for the invasiveness of tumor cells in vitro, causing enhanced EMT and cytoskeleton reconstruction regulated by Ras-related C3 botulinum toxin substrate 1 (RAC1). Reactive Oxygen Species 12-35 Rac family small GTPase 1 Homo sapiens 183-225 32133799-4 2020 DOX-related reactive oxygen species (ROS) were found to be responsible for the invasiveness of tumor cells in vitro, causing enhanced EMT and cytoskeleton reconstruction regulated by Ras-related C3 botulinum toxin substrate 1 (RAC1). Reactive Oxygen Species 12-35 Rac family small GTPase 1 Homo sapiens 227-231 32133799-4 2020 DOX-related reactive oxygen species (ROS) were found to be responsible for the invasiveness of tumor cells in vitro, causing enhanced EMT and cytoskeleton reconstruction regulated by Ras-related C3 botulinum toxin substrate 1 (RAC1). Reactive Oxygen Species 37-40 Rac family small GTPase 1 Homo sapiens 183-225 32133799-4 2020 DOX-related reactive oxygen species (ROS) were found to be responsible for the invasiveness of tumor cells in vitro, causing enhanced EMT and cytoskeleton reconstruction regulated by Ras-related C3 botulinum toxin substrate 1 (RAC1). Reactive Oxygen Species 37-40 Rac family small GTPase 1 Homo sapiens 227-231 31216465-6 2019 PARP-1 catalytic function is required for PARylation of RAC1 at evolutionarily conserved sites in TKI-resistant cells, which restricts NOX-mediated ROS production. Reactive Oxygen Species 148-151 Rac family small GTPase 1 Homo sapiens 56-60 30105917-3 2019 In the pathogenesis of diabetic retinopathy, a progressive disease, reactive oxygen species (ROS) production by activation of a small molecular weight G-protein (Ras-related C3 botulinum toxin substrate 1 [Rac1])-Nox2 signaling precedes mitochondrial damage. Reactive Oxygen Species 68-91 Rac family small GTPase 1 Homo sapiens 206-210 30105917-3 2019 In the pathogenesis of diabetic retinopathy, a progressive disease, reactive oxygen species (ROS) production by activation of a small molecular weight G-protein (Ras-related C3 botulinum toxin substrate 1 [Rac1])-Nox2 signaling precedes mitochondrial damage. Reactive Oxygen Species 93-96 Rac family small GTPase 1 Homo sapiens 162-204 30105917-3 2019 In the pathogenesis of diabetic retinopathy, a progressive disease, reactive oxygen species (ROS) production by activation of a small molecular weight G-protein (Ras-related C3 botulinum toxin substrate 1 [Rac1])-Nox2 signaling precedes mitochondrial damage. Reactive Oxygen Species 93-96 Rac family small GTPase 1 Homo sapiens 206-210 30105917-13 2019 CONCLUSION: Thus, p66Shc has dual role in the development of diabetic retinopathy; its regulation in the early stages of the disease should impede Rac1-ROS production and, in the later stages, prevent mitochondrial damage and initiation of a futile cycle of free radicals. Reactive Oxygen Species 152-155 Rac family small GTPase 1 Homo sapiens 147-151 31035701-2 2019 Rac1, a member of this family, besides its known function in the regulation of actin cytoskeleton, plays a key role in the production of reactive oxygen species, in gene transcription, in DNA repair, and also has been proven to have specific roles in neurons. Reactive Oxygen Species 137-160 Rac family small GTPase 1 Homo sapiens 0-4 31172485-1 2019 The NADPH oxidase complex, responsible for reactive oxygen species (ROS) generation by phagocytes, consists of a membrane-associated flavocytochrome b 558 (a heterodimer of NOX2 and p22phox) and the cytosolic components p47phox, p67phox, Rac(1 or 2), and p40phox. Reactive Oxygen Species 43-66 Rac family small GTPase 1 Homo sapiens 238-248 30787155-2 2019 Reactive oxygen species (ROS) are also regulated by the ubiquitously expressed HACE1 protein (HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1), which targets the Rac1 protein for proteasomal degradation, and this blocks the generation of ROS by Rac1-dependent NADPH oxidases. Reactive Oxygen Species 0-23 Rac family small GTPase 1 Homo sapiens 186-190 30787155-2 2019 Reactive oxygen species (ROS) are also regulated by the ubiquitously expressed HACE1 protein (HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1), which targets the Rac1 protein for proteasomal degradation, and this blocks the generation of ROS by Rac1-dependent NADPH oxidases. Reactive Oxygen Species 0-23 Rac family small GTPase 1 Homo sapiens 269-273 30787155-2 2019 Reactive oxygen species (ROS) are also regulated by the ubiquitously expressed HACE1 protein (HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1), which targets the Rac1 protein for proteasomal degradation, and this blocks the generation of ROS by Rac1-dependent NADPH oxidases. Reactive Oxygen Species 25-28 Rac family small GTPase 1 Homo sapiens 186-190 30787155-2 2019 Reactive oxygen species (ROS) are also regulated by the ubiquitously expressed HACE1 protein (HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1), which targets the Rac1 protein for proteasomal degradation, and this blocks the generation of ROS by Rac1-dependent NADPH oxidases. Reactive Oxygen Species 25-28 Rac family small GTPase 1 Homo sapiens 269-273 30787155-2 2019 Reactive oxygen species (ROS) are also regulated by the ubiquitously expressed HACE1 protein (HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1), which targets the Rac1 protein for proteasomal degradation, and this blocks the generation of ROS by Rac1-dependent NADPH oxidases. Reactive Oxygen Species 262-265 Rac family small GTPase 1 Homo sapiens 186-190 30787155-2 2019 Reactive oxygen species (ROS) are also regulated by the ubiquitously expressed HACE1 protein (HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1), which targets the Rac1 protein for proteasomal degradation, and this blocks the generation of ROS by Rac1-dependent NADPH oxidases. Reactive Oxygen Species 262-265 Rac family small GTPase 1 Homo sapiens 269-273 30553448-5 2019 Rac1 can be activated directly by reactive oxygen species (ROS), by a mechanism distinct from canonical guanine nucleotide exchange factor-driven activation. Reactive Oxygen Species 34-57 Rac family small GTPase 1 Homo sapiens 0-4 30553448-5 2019 Rac1 can be activated directly by reactive oxygen species (ROS), by a mechanism distinct from canonical guanine nucleotide exchange factor-driven activation. Reactive Oxygen Species 59-62 Rac family small GTPase 1 Homo sapiens 0-4 30553448-6 2019 Here we show that loss of ATM kinase activity elevates intracellular ROS, leading to Rac1 activation. Reactive Oxygen Species 69-72 Rac family small GTPase 1 Homo sapiens 85-89 30553448-9 2019 These studies demonstrate a novel mechanism whereby ATM activity and ROS generation regulates Rac1 to modulate pro-migratory cellular behavior. Reactive Oxygen Species 69-72 Rac family small GTPase 1 Homo sapiens 94-98 31172485-1 2019 The NADPH oxidase complex, responsible for reactive oxygen species (ROS) generation by phagocytes, consists of a membrane-associated flavocytochrome b 558 (a heterodimer of NOX2 and p22phox) and the cytosolic components p47phox, p67phox, Rac(1 or 2), and p40phox. Reactive Oxygen Species 68-71 Rac family small GTPase 1 Homo sapiens 238-248 29163784-11 2017 Furthermore, IMP2 expression in these cells correlated with the generation of reactive oxygen species (ROS) and RAC1 expression in BTC cells, suggesting RAC1-induced ROS generation as a potential mechanism of IMP2-promoted progression of GBC. Reactive Oxygen Species 103-106 Rac family small GTPase 1 Homo sapiens 153-157 29462661-10 2018 In summary, the results of our current studies clearly indicate p66Shc also regulates PCa cell migration through ROS-mediated activation of migration-associated proteins, notably Rac1. Reactive Oxygen Species 113-116 Rac family small GTPase 1 Homo sapiens 179-183 29039574-2 2017 Since RAC1 can signal through reactive oxygen species (ROS), we probed the role of the ROS-producing NADPH oxidase (NOX) and p38 mitogen-activated protein kinase (MAPK) in mediating TGF-beta1/RAC1-driven random cell migration (chemokinesis). Reactive Oxygen Species 30-53 Rac family small GTPase 1 Homo sapiens 6-10 29163784-11 2017 Furthermore, IMP2 expression in these cells correlated with the generation of reactive oxygen species (ROS) and RAC1 expression in BTC cells, suggesting RAC1-induced ROS generation as a potential mechanism of IMP2-promoted progression of GBC. Reactive Oxygen Species 78-101 Rac family small GTPase 1 Homo sapiens 153-157 30279516-2 2019 The major source of ROS in intestinal epithelial cells is the NADPH oxidase NOX1, which consists of the transmembrane proteins, NOX1 and p22PHOX, and the cytosolic proteins, NOXO1, NOXA1, and Rac1. Reactive Oxygen Species 20-23 Rac family small GTPase 1 Homo sapiens 192-196 30396896-7 2019 Furthermore, SL accelerated the recruitment of Rac1 to the cell membrane, leading to the generation of reactive oxygen species for the elimination of phagocytosed bacteria. Reactive Oxygen Species 103-126 Rac family small GTPase 1 Homo sapiens 47-51 29186971-5 2018 Studies have thus identified (onco)proteins (Bcl-2, STAT3/5, RAS, Rac1, and Myc) in manipulating ROS level as well as exploiting an altered redox environment to create a milieu conducive for cancer formation and progression. Reactive Oxygen Species 97-100 Rac family small GTPase 1 Homo sapiens 66-70 29740674-7 2018 Knockdown of Rac1 decreases ROS production in DA-MED-treated cells, resulting in a concomitant decrease in DA-MED-induced apoptosis. Reactive Oxygen Species 28-31 Rac family small GTPase 1 Homo sapiens 13-17 29330095-0 2018 Crosstalk between Rac1-mediated actin regulation and ROS production. Reactive Oxygen Species 53-56 Rac family small GTPase 1 Homo sapiens 18-22 29330095-2 2018 Remarkably, another event that is completely different from those related to actin regulation has the same relevance; the Rac1-mediated production of reactive oxygen species (ROS) through NADPH oxidases (NOX). Reactive Oxygen Species 150-173 Rac family small GTPase 1 Homo sapiens 122-126 29330095-2 2018 Remarkably, another event that is completely different from those related to actin regulation has the same relevance; the Rac1-mediated production of reactive oxygen species (ROS) through NADPH oxidases (NOX). Reactive Oxygen Species 175-178 Rac family small GTPase 1 Homo sapiens 122-126 29330095-3 2018 Each outcome involves different Rac1 downstream effectors; on one hand, events related to the actin cytoskeleton require Rac1 to bind to WAVEs proteins and PAKs that ultimately promote actin branching and turnover, on the other, NOX-derived ROS production demands active Rac1 to be bound to a cytosolic activator of NOX. Reactive Oxygen Species 241-244 Rac family small GTPase 1 Homo sapiens 32-36 29330095-3 2018 Each outcome involves different Rac1 downstream effectors; on one hand, events related to the actin cytoskeleton require Rac1 to bind to WAVEs proteins and PAKs that ultimately promote actin branching and turnover, on the other, NOX-derived ROS production demands active Rac1 to be bound to a cytosolic activator of NOX. Reactive Oxygen Species 241-244 Rac family small GTPase 1 Homo sapiens 121-125 29330095-3 2018 Each outcome involves different Rac1 downstream effectors; on one hand, events related to the actin cytoskeleton require Rac1 to bind to WAVEs proteins and PAKs that ultimately promote actin branching and turnover, on the other, NOX-derived ROS production demands active Rac1 to be bound to a cytosolic activator of NOX. Reactive Oxygen Species 241-244 Rac family small GTPase 1 Homo sapiens 121-125 29330095-4 2018 How Rac1-mediated signaling ends up promoting actin-related events, NOX-derived ROS, or both is poorly understood. Reactive Oxygen Species 80-83 Rac family small GTPase 1 Homo sapiens 4-8 29330095-6 2018 Hence, evidence of Rac1 regulatory events leading to both actin remodeling and NOX-mediated ROS generation are discussed. Reactive Oxygen Species 92-95 Rac family small GTPase 1 Homo sapiens 19-23 29330095-8 2018 Together, discussed evidence shed light on cellular mechanisms which requires Rac1 to direct either actin- and/or ROS-related events, helping to understand crucial roles of Rac1 dual functionality. Reactive Oxygen Species 114-117 Rac family small GTPase 1 Homo sapiens 78-82 29330095-8 2018 Together, discussed evidence shed light on cellular mechanisms which requires Rac1 to direct either actin- and/or ROS-related events, helping to understand crucial roles of Rac1 dual functionality. Reactive Oxygen Species 114-117 Rac family small GTPase 1 Homo sapiens 173-177 29039574-2 2017 Since RAC1 can signal through reactive oxygen species (ROS), we probed the role of the ROS-producing NADPH oxidase (NOX) and p38 mitogen-activated protein kinase (MAPK) in mediating TGF-beta1/RAC1-driven random cell migration (chemokinesis). Reactive Oxygen Species 55-58 Rac family small GTPase 1 Homo sapiens 6-10 29039574-2 2017 Since RAC1 can signal through reactive oxygen species (ROS), we probed the role of the ROS-producing NADPH oxidase (NOX) and p38 mitogen-activated protein kinase (MAPK) in mediating TGF-beta1/RAC1-driven random cell migration (chemokinesis). Reactive Oxygen Species 87-90 Rac family small GTPase 1 Homo sapiens 6-10 29039574-2 2017 Since RAC1 can signal through reactive oxygen species (ROS), we probed the role of the ROS-producing NADPH oxidase (NOX) and p38 mitogen-activated protein kinase (MAPK) in mediating TGF-beta1/RAC1-driven random cell migration (chemokinesis). Reactive Oxygen Species 87-90 Rac family small GTPase 1 Homo sapiens 192-196 29039574-5 2017 To analyze whether RAC1 functions through NOX and ROS to promote cell motility, we performed real-time cell migration assays with xCELLigence technology in the presence of the ROS scavenger N-acetyl-L-cysteine (NAC) and various NOX inhibitors. Reactive Oxygen Species 50-53 Rac family small GTPase 1 Homo sapiens 19-23 29039574-5 2017 To analyze whether RAC1 functions through NOX and ROS to promote cell motility, we performed real-time cell migration assays with xCELLigence technology in the presence of the ROS scavenger N-acetyl-L-cysteine (NAC) and various NOX inhibitors. Reactive Oxygen Species 177-180 Rac family small GTPase 1 Homo sapiens 19-23 29039574-8 2017 Our data suggest that TGF-beta1-induced chemokinesis in PDAC cells is mediated through a RAC1/NOX4/ROS/p38 MAPK cascade. Reactive Oxygen Species 99-102 Rac family small GTPase 1 Homo sapiens 89-93 29163784-11 2017 Furthermore, IMP2 expression in these cells correlated with the generation of reactive oxygen species (ROS) and RAC1 expression in BTC cells, suggesting RAC1-induced ROS generation as a potential mechanism of IMP2-promoted progression of GBC. Reactive Oxygen Species 166-169 Rac family small GTPase 1 Homo sapiens 153-157 27380043-8 2017 In addition, TMP could notably down-regulate the characteristic proteins in Rho/ROCK signaling pathway such as RhoA and Rac1, which triggered abnormal changes of eNOS and ROS, respectively. Reactive Oxygen Species 171-174 Rac family small GTPase 1 Homo sapiens 120-124 26795736-2 2016 The current assumed signaling cascade from RANK to ROS production is RANK, TRAF6, Rac1, and then Nox. Reactive Oxygen Species 51-54 Rac family small GTPase 1 Homo sapiens 82-86 27681226-0 2016 RhoA and Rac1 GTPases Differentially Regulate Agonist-Receptor Mediated Reactive Oxygen Species Generation in Platelets. Reactive Oxygen Species 72-95 Rac family small GTPase 1 Homo sapiens 9-13 27681226-2 2016 RhoA and Rac1 GTPases are involved in ROS generation by NOX in a variety of cells, but their roles in platelet ROS production remain unclear. Reactive Oxygen Species 38-41 Rac family small GTPase 1 Homo sapiens 9-13 27681226-2 2016 RhoA and Rac1 GTPases are involved in ROS generation by NOX in a variety of cells, but their roles in platelet ROS production remain unclear. Reactive Oxygen Species 111-114 Rac family small GTPase 1 Homo sapiens 9-13 27681226-5 2016 Conditional deletion of RhoA or Rac1 gene inhibited thrombin induced ROS generation in platelets. Reactive Oxygen Species 69-72 Rac family small GTPase 1 Homo sapiens 32-36 28098862-0 2017 Rhein suppresses matrix metalloproteinase production by regulating the Rac1/ROS/MAPK/AP-1 pathway in human ovarian carcinoma cells. Reactive Oxygen Species 76-79 Rac family small GTPase 1 Homo sapiens 71-75 28098862-2 2017 Rac1 proteins might mostly influence cell migration and invasion by generating endogenous reactive oxygen species. Reactive Oxygen Species 90-113 Rac family small GTPase 1 Homo sapiens 0-4 27656113-6 2017 Introducing constitutively activated RAC1 disrupted cell polarity and increased ROS levels, indicating that RAC1 is a crucial regulator that links cell polarity and ROS generation. Reactive Oxygen Species 80-83 Rac family small GTPase 1 Homo sapiens 37-41 27656113-6 2017 Introducing constitutively activated RAC1 disrupted cell polarity and increased ROS levels, indicating that RAC1 is a crucial regulator that links cell polarity and ROS generation. Reactive Oxygen Species 80-83 Rac family small GTPase 1 Homo sapiens 108-112 27656113-6 2017 Introducing constitutively activated RAC1 disrupted cell polarity and increased ROS levels, indicating that RAC1 is a crucial regulator that links cell polarity and ROS generation. Reactive Oxygen Species 165-168 Rac family small GTPase 1 Homo sapiens 37-41 27656113-6 2017 Introducing constitutively activated RAC1 disrupted cell polarity and increased ROS levels, indicating that RAC1 is a crucial regulator that links cell polarity and ROS generation. Reactive Oxygen Species 165-168 Rac family small GTPase 1 Homo sapiens 108-112 27779078-4 2017 However, it is becoming increasingly clear that prolonged exposure of beta-cells to hyperglycemic conditions, leads to sustained activation of Rac1-Nox2 signaling axis culminating in excessive generation of intracellular ROS (oxidative stress) and beta-cell dysregulation and demise. Reactive Oxygen Species 221-224 Rac family small GTPase 1 Homo sapiens 143-147 27779078-9 2017 We have provided an overview of existing evidence in the islet beta-cell on the regulatory roles of these MAPKs in mediating cellular responses to alterations in intracellularly generated ROS, which is mediated by the Rac1-Nox2 signaling module. Reactive Oxygen Species 188-191 Rac family small GTPase 1 Homo sapiens 218-222 27681226-6 2016 Addition of Y27632, a RhoA inhibitor, NSC23766 or Phox-I, an inhibitor of Rac1-p67phox interaction, to human platelets blocked thrombin induced ROS generation. Reactive Oxygen Species 144-147 Rac family small GTPase 1 Homo sapiens 74-78 27681226-7 2016 These data suggest that: (a) RhoA/ROCK/p47phox signaling axis promotes ROS production that, at least in part, contributes to platelet activation in conjunction with or independent of the RhoA/ROCK mediated phosphorylation of MLC; and (b) RhoA and Rac1 differentially regulate ROS generation by inhibiting phosphorylation of p47phox and Rac1-p67phox interaction, respectively. Reactive Oxygen Species 71-74 Rac family small GTPase 1 Homo sapiens 247-251 27681226-7 2016 These data suggest that: (a) RhoA/ROCK/p47phox signaling axis promotes ROS production that, at least in part, contributes to platelet activation in conjunction with or independent of the RhoA/ROCK mediated phosphorylation of MLC; and (b) RhoA and Rac1 differentially regulate ROS generation by inhibiting phosphorylation of p47phox and Rac1-p67phox interaction, respectively. Reactive Oxygen Species 71-74 Rac family small GTPase 1 Homo sapiens 336-340 26426686-11 2015 p62 induced this ROS production by a DLK1-dependent induction and activation of the small Rho-GTPase RAC1, activating NADPH oxidase and being overexpressed in human HCC. Reactive Oxygen Species 17-20 Rac family small GTPase 1 Homo sapiens 101-105 26476350-10 2015 These findings provide evidence that active Rap1a inhibits TNF-alpha-induced CEC migration by inhibiting NADPH oxidase-dependent NF-kappaB and Rac1 activation and suggests that Rap1a de-escalates CNV development by interfering with ROS-dependent signaling in several steps of the pathogenic process. Reactive Oxygen Species 232-235 Rac family small GTPase 1 Homo sapiens 143-147 27048259-0 2016 Actin depolymerization mediated loss of SNTA1 phosphorylation and Rac1 activity has implications on ROS production, cell migration and apoptosis. Reactive Oxygen Species 100-103 Rac family small GTPase 1 Homo sapiens 66-70 27048259-10 2016 The loss of SNTA1tyrosine phosphorylation and Rac1 activity by actin depolymerization results in increased apoptosis, decreased cell migration and decreased reactive oxygen species (ROS) levels in breast carcinoma cells. Reactive Oxygen Species 157-180 Rac family small GTPase 1 Homo sapiens 46-50 27048259-10 2016 The loss of SNTA1tyrosine phosphorylation and Rac1 activity by actin depolymerization results in increased apoptosis, decreased cell migration and decreased reactive oxygen species (ROS) levels in breast carcinoma cells. Reactive Oxygen Species 182-185 Rac family small GTPase 1 Homo sapiens 46-50 25249940-3 2014 Rac1 is also a crucial regulator of NADPH-dependent membrane oxidase (NOX), a prominent source of reactive oxygen species (ROS), thus having a central role in the inflammatory response and neurotoxicity mediated by microglia cells in the nervous system. Reactive Oxygen Species 98-121 Rac family small GTPase 1 Homo sapiens 0-4 26079889-3 2015 Noteworthy, we have previously demonstrated that EGFR/Rac1/reactive oxygen species (ROS)/matrix metalloproteinase 9 (MMP-9) is a key signaling cascade regulating MUC5AC production in airway cells challenged with LPS. Reactive Oxygen Species 59-82 Rac family small GTPase 1 Homo sapiens 54-58 25677088-4 2015 Rac1 responds to extracellular signals and is involved in cytoskeletal rearrangement, reactive oxygen species generation and cell cycle progression. Reactive Oxygen Species 86-109 Rac family small GTPase 1 Homo sapiens 0-4 25249940-3 2014 Rac1 is also a crucial regulator of NADPH-dependent membrane oxidase (NOX), a prominent source of reactive oxygen species (ROS), thus having a central role in the inflammatory response and neurotoxicity mediated by microglia cells in the nervous system. Reactive Oxygen Species 123-126 Rac family small GTPase 1 Homo sapiens 0-4 24434436-8 2014 In addition, the SNTA1/P66shc-mediated Rac1 activation resulted in an increase in reactive oxygen species (ROS) production and migratory potential in human breast cancer cells. Reactive Oxygen Species 82-105 Rac family small GTPase 1 Homo sapiens 39-43 24554007-3 2014 Activation of Ras-related C3 botulinum toxin substrate 1 (RAC1), a NOX2 holoenzyme member, is necessary for NOX2 activation and ROS generation. Reactive Oxygen Species 128-131 Rac family small GTPase 1 Homo sapiens 14-56 24554007-3 2014 Activation of Ras-related C3 botulinum toxin substrate 1 (RAC1), a NOX2 holoenzyme member, is necessary for NOX2 activation and ROS generation. Reactive Oxygen Species 128-131 Rac family small GTPase 1 Homo sapiens 58-62 24554007-11 2014 CONCLUSIONS/INTERPRETATION: The TIAM1-RAC1-NOX2 signalling axis is activated in the initial stages of diabetes to increase intracellular ROS leading to mitochondrial damage and accelerated capillary cell apoptosis. Reactive Oxygen Species 137-140 Rac family small GTPase 1 Homo sapiens 38-42 23919665-4 2014 RECENT ADVANCES: Rac1 GTPase is an established master regulator of cell motility through the cortical actin reorganization and of reactive oxygen species generation through the regulation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity. Reactive Oxygen Species 130-153 Rac family small GTPase 1 Homo sapiens 17-21 24434436-8 2014 In addition, the SNTA1/P66shc-mediated Rac1 activation resulted in an increase in reactive oxygen species (ROS) production and migratory potential in human breast cancer cells. Reactive Oxygen Species 107-110 Rac family small GTPase 1 Homo sapiens 39-43 24434436-9 2014 CONCLUSION: Together, our results present a possible mechanism of Rac1 activation involving SNTA1 and emphasise its role in ROS generation, cell migration, and acquisition of malignancy. Reactive Oxygen Species 124-127 Rac family small GTPase 1 Homo sapiens 66-70 24583638-6 2014 We also show that oncogenic Ras-induced ROS are produced in a Rac1 and NADPH oxidase (Nox4)-dependent manner. Reactive Oxygen Species 40-43 Rac family small GTPase 1 Homo sapiens 62-66 23612479-8 2013 In turn Rac1-GTP mediates an increase in ROS levels via nuclear membrane-associated NADPH oxidase type 4. Reactive Oxygen Species 41-44 Rac family small GTPase 1 Homo sapiens 8-12 24064382-5 2013 Here we report that Axl activation elicits ROS accumulation through the oxidase-coupled small GTPase Rac1. Reactive Oxygen Species 43-46 Rac family small GTPase 1 Homo sapiens 101-105 23711511-6 2013 RESULTS: ROS generation in either J774 or HEK293 cells (expressing P2X7, NOX2, Rac1, p47phox and p67phox) was strictly dependent on calcium entry via P2X7R. Reactive Oxygen Species 9-12 Rac family small GTPase 1 Homo sapiens 79-83 23608189-3 2013 Exposure of HAECs to TNF-alpha caused production of ROS via Rac-1 membrane translocation and activation. Reactive Oxygen Species 52-55 Rac family small GTPase 1 Homo sapiens 60-65 23733346-4 2013 Here, we identify a novel polarity complex that directs localized Rac1 activation required for downstream reactive oxygen species (ROS) production. Reactive Oxygen Species 106-129 Rac family small GTPase 1 Homo sapiens 66-70 23733346-4 2013 Here, we identify a novel polarity complex that directs localized Rac1 activation required for downstream reactive oxygen species (ROS) production. Reactive Oxygen Species 131-134 Rac family small GTPase 1 Homo sapiens 66-70 23465490-4 2013 The results revealed that platelet derived growth factor (PDGF) can induce ROS production at FA sites, which is mediated by Rac1 activation. Reactive Oxygen Species 75-78 Rac family small GTPase 1 Homo sapiens 124-128 22746102-4 2013 RESULTS: Signaling by the KSHV early lytic gene viral G protein-coupled receptor (vGPCR) activated ROS production in mECK36 cells via a Rac1-NADPH oxidase pathway. Reactive Oxygen Species 99-102 Rac family small GTPase 1 Homo sapiens 136-140 23637767-12 2013 Thus, Ac2-26 peptide inhibits TNFalpha-activated, Rac1-dependent NADPH oxidase derived ROS formation, attenuates NFkappaB pathways and ICAM-1 and VCAM-1 expression in endothelial cells. Reactive Oxygen Species 87-90 Rac family small GTPase 1 Homo sapiens 50-54 23322165-1 2013 Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Reactive Oxygen Species 0-23 Rac family small GTPase 1 Homo sapiens 250-254 23322165-1 2013 Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1. Reactive Oxygen Species 25-28 Rac family small GTPase 1 Homo sapiens 250-254 23461363-0 2013 P66Shc-rac1 pathway-mediated ROS production and cell migration is downregulated by ascorbic acid. Reactive Oxygen Species 29-32 Rac family small GTPase 1 Homo sapiens 7-11 23375814-8 2013 Furthermore, overexpression of dominant-negative human Rac-1 mutant mimicked the effects of PEDF on ROS generation and Mcl-1 expression in U266 cells. Reactive Oxygen Species 100-103 Rac family small GTPase 1 Homo sapiens 55-60 22358380-2 2013 RAC1 activates the nicotinamide adenine dinucleotide phosphate oxidase complex which promotes formation of reactive oxygen species and degradation enzymes. Reactive Oxygen Species 107-130 Rac family small GTPase 1 Homo sapiens 0-4 22746102-2 2013 Rac1-activated reactive oxygen species (ROS) production has been implicated in KS tumorigenesis. Reactive Oxygen Species 15-38 Rac family small GTPase 1 Homo sapiens 0-4 22746102-2 2013 Rac1-activated reactive oxygen species (ROS) production has been implicated in KS tumorigenesis. Reactive Oxygen Species 40-43 Rac family small GTPase 1 Homo sapiens 0-4 23223568-5 2013 Poly-Ub/BGIN interactions support BGIN-mediated inactivation of a membranous Rac1 population, which consequently inactivates membrane-localized Rac1 effector systems such as reactive oxygen species (ROS) generation by the Nox1 complex. Reactive Oxygen Species 174-197 Rac family small GTPase 1 Homo sapiens 77-81 23223568-5 2013 Poly-Ub/BGIN interactions support BGIN-mediated inactivation of a membranous Rac1 population, which consequently inactivates membrane-localized Rac1 effector systems such as reactive oxygen species (ROS) generation by the Nox1 complex. Reactive Oxygen Species 174-197 Rac family small GTPase 1 Homo sapiens 144-148 23223568-5 2013 Poly-Ub/BGIN interactions support BGIN-mediated inactivation of a membranous Rac1 population, which consequently inactivates membrane-localized Rac1 effector systems such as reactive oxygen species (ROS) generation by the Nox1 complex. Reactive Oxygen Species 199-202 Rac family small GTPase 1 Homo sapiens 77-81 23223568-5 2013 Poly-Ub/BGIN interactions support BGIN-mediated inactivation of a membranous Rac1 population, which consequently inactivates membrane-localized Rac1 effector systems such as reactive oxygen species (ROS) generation by the Nox1 complex. Reactive Oxygen Species 199-202 Rac family small GTPase 1 Homo sapiens 144-148 23864022-0 2013 Hace1 controls ROS generation of vertebrate Rac1-dependent NADPH oxidase complexes. Reactive Oxygen Species 15-18 Rac family small GTPase 1 Homo sapiens 44-48 23864022-3 2013 This event blocks de novo reactive oxygen species generation by Rac1-dependent NADPH oxidases, and thereby confers cellular protection from reactive oxygen species-induced DNA damage and cyclin D1-driven hyper-proliferation. Reactive Oxygen Species 26-49 Rac family small GTPase 1 Homo sapiens 64-68 23864022-3 2013 This event blocks de novo reactive oxygen species generation by Rac1-dependent NADPH oxidases, and thereby confers cellular protection from reactive oxygen species-induced DNA damage and cyclin D1-driven hyper-proliferation. Reactive Oxygen Species 140-163 Rac family small GTPase 1 Homo sapiens 64-68 23864022-5 2013 Our data reveal a conserved ubiquitin-dependent molecular mechanism that controls the activity of Rac1-dependent NADPH oxidase complexes, and thus constitutes the first known example of a tumor suppressor protein that directly regulates reactive oxygen species production in vertebrates. Reactive Oxygen Species 237-260 Rac family small GTPase 1 Homo sapiens 98-102 22286230-0 2012 Dieckol from Ecklonia cava suppresses the migration and invasion of HT1080 cells by inhibiting the focal adhesion kinase pathway downstream of Rac1-ROS signaling. Reactive Oxygen Species 148-151 Rac family small GTPase 1 Homo sapiens 143-147 23014943-6 2012 Thrombin enhanced the formation of NO as well as ROS generation involving the GTPase Rac1 in endothelial cells. Reactive Oxygen Species 49-52 Rac family small GTPase 1 Homo sapiens 85-89 23014943-7 2012 Rac1-dependent ROS formation promoted induction of HIF-1alpha, PAI-1 and capillary formation by thrombin, while NO reduced ROS bioavailability and subsequently limited induction of HIF-1alpha, PAI-1 and the angiogenic response. Reactive Oxygen Species 15-18 Rac family small GTPase 1 Homo sapiens 0-4 23014943-7 2012 Rac1-dependent ROS formation promoted induction of HIF-1alpha, PAI-1 and capillary formation by thrombin, while NO reduced ROS bioavailability and subsequently limited induction of HIF-1alpha, PAI-1 and the angiogenic response. Reactive Oxygen Species 123-126 Rac family small GTPase 1 Homo sapiens 0-4 23014943-8 2012 Importantly, thrombin activation of Rac1 was diminished by NO, but enhanced by ROS. Reactive Oxygen Species 79-82 Rac family small GTPase 1 Homo sapiens 36-40 23014943-9 2012 Thus, our findings show that capillary formation induced by thrombin via Rac1-dependent activation of HIF-1 and PAI-1 is limited by the concomitant release of NO which reduced ROS bioavailability. Reactive Oxygen Species 176-179 Rac family small GTPase 1 Homo sapiens 73-77 23014943-10 2012 Rac1 activity is sensitive to ROS and NO, thereby playing an essential role in fine tuning the endothelial response to thrombin. Reactive Oxygen Species 30-33 Rac family small GTPase 1 Homo sapiens 0-4 22335598-6 2012 Concomitantly, translocation of Rac1 to the plasma membrane, which leads to the activation of NADPH oxidases and generation of ROS, was significantly attenuated. Reactive Oxygen Species 127-130 Rac family small GTPase 1 Homo sapiens 32-36 22286230-10 2012 These results suggest that the Rac1-ROS-linked cascade enhances migration and invasion of HT1080 cells by inducing expression of MMPs through activation of the FAK signaling pathway, whereas dieckol downregulates FAK signaling through scavenging intracellular ROS. Reactive Oxygen Species 36-39 Rac family small GTPase 1 Homo sapiens 31-35 22286230-10 2012 These results suggest that the Rac1-ROS-linked cascade enhances migration and invasion of HT1080 cells by inducing expression of MMPs through activation of the FAK signaling pathway, whereas dieckol downregulates FAK signaling through scavenging intracellular ROS. Reactive Oxygen Species 260-263 Rac family small GTPase 1 Homo sapiens 31-35 22519881-0 2012 Activation of PPARdelta counteracts angiotensin II-induced ROS generation by inhibiting rac1 translocation in vascular smooth muscle cells. Reactive Oxygen Species 59-62 Rac family small GTPase 1 Homo sapiens 88-92 22519881-7 2012 Ligand-activated PPARdelta also blocked Ang II-induced translocation of Rac1 to the cell membrane, inhibiting the activation of NADPH oxidases and consequently ROS generation. Reactive Oxygen Species 160-163 Rac family small GTPase 1 Homo sapiens 72-76 22101521-3 2012 We have shown that ROS derived from Rac1-dependent NADPH oxidase are involved in VEGFR2 autophosphorylation and angiogenic-related responses in ECs. Reactive Oxygen Species 19-22 Rac family small GTPase 1 Homo sapiens 36-40 22286230-5 2012 H2O2 or integrin signal-mediated ROS generation increases migration and invasion of HT1080 cells, which correlates with Rac1 activation and increased expression and phosphorylation of focal adhesion kinase (FAK). Reactive Oxygen Species 33-36 Rac family small GTPase 1 Homo sapiens 120-124 22286230-6 2012 Rac1 activation is required for ROS generation. Reactive Oxygen Species 32-35 Rac family small GTPase 1 Homo sapiens 0-4 22286230-7 2012 Depletion of FAK by siRNA suppresses Rac1-ROS-induced cell migration and invasion. Reactive Oxygen Species 42-45 Rac family small GTPase 1 Homo sapiens 37-41 22153388-5 2012 Atorvastatin inhibited ROS generation partly through suppression of Rac1/NADPH oxidase activity. Reactive Oxygen Species 23-26 Rac family small GTPase 1 Homo sapiens 68-72 22153388-7 2012 Thus, inhibition of ROS production by concomitant suppression of Rac1/NADPH oxidase activity and upregulation of the activity of GPx and catalase contributes critically to atorvastatin-reduced VEGF expression in NSCLCs. Reactive Oxygen Species 20-23 Rac family small GTPase 1 Homo sapiens 65-69 22237206-0 2012 DNA damage induces reactive oxygen species generation through the H2AX-Nox1/Rac1 pathway. Reactive Oxygen Species 19-42 Rac family small GTPase 1 Homo sapiens 76-80 22237206-3 2012 Increased levels of ROS and cell death induced by H2AX overexpression alone or DNA damage leading to H2AX accumulation are reduced by treating cells with the antioxidant N-Acetyl-L-Cysteine (NAC), the NADP(H) oxidase (Nox) inhibitor DPI, expression of Rac1N17, and knockdown of Nox1, but not Nox4, indicating that induction of ROS by H2AX is mediated through Nox1 and Rac1 GTPase. Reactive Oxygen Species 20-23 Rac family small GTPase 1 Homo sapiens 252-256 22237206-3 2012 Increased levels of ROS and cell death induced by H2AX overexpression alone or DNA damage leading to H2AX accumulation are reduced by treating cells with the antioxidant N-Acetyl-L-Cysteine (NAC), the NADP(H) oxidase (Nox) inhibitor DPI, expression of Rac1N17, and knockdown of Nox1, but not Nox4, indicating that induction of ROS by H2AX is mediated through Nox1 and Rac1 GTPase. Reactive Oxygen Species 327-330 Rac family small GTPase 1 Homo sapiens 252-256 22144277-1 2012 Rac, a member of the Rho family small GTPases, plays a crucial role in activation of Nox family NADPH oxidases in animals, enzymes dedicated to production of reactive oxygen species such as superoxide. Reactive Oxygen Species 158-181 Rac family small GTPase 1 Homo sapiens 0-3 21660950-2 2011 ROS can be produced in response to integrin ligation and growth factor stimulation through Rac1 and its effector protein NADPH oxidase. Reactive Oxygen Species 0-3 Rac family small GTPase 1 Homo sapiens 91-95 21321939-5 2011 EV71-induced ROS generation was mediated through activation of integrin beta1, an epidermal growth factor receptor (EGFR), Rac1 and NADPH oxidase which revealed by using selective pharmacological inhibitors or transfection with respective siRNAs. Reactive Oxygen Species 13-16 Rac family small GTPase 1 Homo sapiens 123-127 21773684-12 2011 Glucose-induced ROS production was quenched by C-peptide and this was associated with a decreased NAD(P)H oxidase activity and reduced RAC-1 membrane production and GTPase activity. Reactive Oxygen Species 16-19 Rac family small GTPase 1 Homo sapiens 135-140 21302299-7 2011 These findings indicate that NRG-induced HaCaT cell migration via the ROS-SSH-1L-cofilin pathway is activated as a consequence of Rac1 and Nox activation. Reactive Oxygen Species 70-73 Rac family small GTPase 1 Homo sapiens 130-134 21200133-1 2011 Previously, we reported that CD40-induced production of reactive oxygen species (ROS) by NADPH oxidase requires the TNF receptor-associated factor (TRAF) 3, as well as the activities of phosphatidylinositol 3-kinase (PI3K) and Rac1. Reactive Oxygen Species 56-79 Rac family small GTPase 1 Homo sapiens 227-231 21620958-0 2011 beta1-Integrin is up-regulated via Rac1-dependent reactive oxygen species as part of the hypertrophic cardiomyocyte response. Reactive Oxygen Species 50-73 Rac family small GTPase 1 Homo sapiens 35-39 21620958-6 2011 Further, ET-1 increased beta(1)-integrin mRNA and protein expression via Rac1-ROS-dependent MEK/ERK and EGF receptor-PI3K/Akt activation as shown by adenoviral dominant-negative Rac1 or overexpression of copper/zinc-superoxide dismutase. Reactive Oxygen Species 78-81 Rac family small GTPase 1 Homo sapiens 73-77 21620958-6 2011 Further, ET-1 increased beta(1)-integrin mRNA and protein expression via Rac1-ROS-dependent MEK/ERK and EGF receptor-PI3K/Akt activation as shown by adenoviral dominant-negative Rac1 or overexpression of copper/zinc-superoxide dismutase. Reactive Oxygen Species 78-81 Rac family small GTPase 1 Homo sapiens 178-182 21620958-9 2011 In conclusion, beta(1)-integrin up-regulation in response to ET-1 is mediated via Rac1-ROS-dependent activation of prohypertrophic pathways and is mandatory for ET-1-induced FAK activation, cell adhesion, and hypertrophic response. Reactive Oxygen Species 87-90 Rac family small GTPase 1 Homo sapiens 82-86 21507984-8 2011 Based on these results, we concluded that Rac1-dependent NOX1 activity is required for RV- or poly(I:C)-induced ROS generation, which in turn disrupts the barrier function of polarized airway epithelia. Reactive Oxygen Species 112-115 Rac family small GTPase 1 Homo sapiens 42-46 21200133-1 2011 Previously, we reported that CD40-induced production of reactive oxygen species (ROS) by NADPH oxidase requires the TNF receptor-associated factor (TRAF) 3, as well as the activities of phosphatidylinositol 3-kinase (PI3K) and Rac1. Reactive Oxygen Species 81-84 Rac family small GTPase 1 Homo sapiens 227-231 21200133-4 2011 Our studies in Raji human B lymphomas revealed that CD40-induced ROS production by 5-LO also requires the activities of PI3K and Rac1. Reactive Oxygen Species 65-68 Rac family small GTPase 1 Homo sapiens 129-133 27795668-10 2011 Once activated, Rac1 aggregates with subunits of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, resulting in the generation of reactive oxygen species. Reactive Oxygen Species 141-164 Rac family small GTPase 1 Homo sapiens 16-20 21980400-8 2011 N-acetyl-L-cysteine, a scavenger of ROS, inhibited hypoxia-induced ROS generation, PI3K, ERK and Rac1 activation as well as HIF-1alpha expression. Reactive Oxygen Species 36-39 Rac family small GTPase 1 Homo sapiens 97-101 20001745-5 2010 PAK-1 and Rac1 were activated by thrombin involving calcium, thus resulting in enhanced generation of reactive oxygen species (ROS) in human pulmonary artery smooth muscle cells (PASMCs). Reactive Oxygen Species 102-125 Rac family small GTPase 1 Homo sapiens 10-14 20510204-3 2010 The enzyme responsible for ROS generation is called NADPH oxidase, or respiratory burst oxidase, and is composed of six proteins: gp91phox, p22phox, p47phox, p67phox, p40phox and Rac1/2. Reactive Oxygen Species 27-30 Rac family small GTPase 1 Homo sapiens 179-185 20001745-5 2010 PAK-1 and Rac1 were activated by thrombin involving calcium, thus resulting in enhanced generation of reactive oxygen species (ROS) in human pulmonary artery smooth muscle cells (PASMCs). Reactive Oxygen Species 127-130 Rac family small GTPase 1 Homo sapiens 10-14 20001745-8 2010 Thus, PAK-1 and its activator Rac1 are novel HIF-1 targets that may constitute a positive-feedback loop for induction of HIF-1alpha by thrombin and ROS, thus explaining elevated levels of PAK-1, Rac1, and HIF-1alpha in remodeled pulmonary vessels. Reactive Oxygen Species 148-151 Rac family small GTPase 1 Homo sapiens 30-34 20001745-8 2010 Thus, PAK-1 and its activator Rac1 are novel HIF-1 targets that may constitute a positive-feedback loop for induction of HIF-1alpha by thrombin and ROS, thus explaining elevated levels of PAK-1, Rac1, and HIF-1alpha in remodeled pulmonary vessels. Reactive Oxygen Species 148-151 Rac family small GTPase 1 Homo sapiens 195-199 20097180-7 2010 Furthermore, we observed that these small molecules blocked LTB4-induced chemotaxis by inhibiting the BLT2-PI3K/Akt-downstream, Rac1-reactive oxygen species-dependent pathway. Reactive Oxygen Species 133-156 Rac family small GTPase 1 Homo sapiens 128-132 20403426-7 2010 Furthermore, expression of Rac1 N17, a dominant negative mutant of Rac1, a member of the Rho family of small GTPases, suppressed VEGF-induced ROS generation and CD146 dimerization. Reactive Oxygen Species 142-145 Rac family small GTPase 1 Homo sapiens 27-31 20403426-7 2010 Furthermore, expression of Rac1 N17, a dominant negative mutant of Rac1, a member of the Rho family of small GTPases, suppressed VEGF-induced ROS generation and CD146 dimerization. Reactive Oxygen Species 142-145 Rac family small GTPase 1 Homo sapiens 67-71 20231105-1 2010 The small Rho GTPases Rac1 and Rac2 regulate actin structures and mediate reactive oxygen species (ROS) production via NADPH oxidase in a variety of cells. Reactive Oxygen Species 74-97 Rac family small GTPase 1 Homo sapiens 22-26 20231105-1 2010 The small Rho GTPases Rac1 and Rac2 regulate actin structures and mediate reactive oxygen species (ROS) production via NADPH oxidase in a variety of cells. Reactive Oxygen Species 99-102 Rac family small GTPase 1 Homo sapiens 22-26 20070306-6 2010 Whereas Rac1 activation occurred during GAS invasion, ROS production in GAS-infected cells was clearly inhibited by transfection with the Rac1 mutants (L37 or V12L37), but not by the dominant active mutant (V12L61) or by the dominant negative mutant (N17). Reactive Oxygen Species 54-57 Rac family small GTPase 1 Homo sapiens 138-142 20070306-7 2010 These observations indicate that GAS invasion triggers ROS production through Rac1 activation and generated ROS induced mitochondrial dysfunction leading to cellular apoptosis. Reactive Oxygen Species 55-58 Rac family small GTPase 1 Homo sapiens 78-82 20153729-6 2010 Our results also indicate that signaling events involved in H-R-enhanced PANC-1 invasiveness comprehend PI3K-dependent activation of Rac1, which mediated the formation of NADPH-generated reactive oxygen species responsible for MMP-2 secretion and activation. Reactive Oxygen Species 187-210 Rac family small GTPase 1 Homo sapiens 133-137 19633358-7 2009 Knockdown of Rac1 inhibited VEGF-induced ROS production consistent with Rac lying upstream of ROS in this pathway. Reactive Oxygen Species 41-44 Rac family small GTPase 1 Homo sapiens 13-17 20062930-8 2010 While Rac1 enforces the endothelial junctions, it becomes part of a barrier-disturbing mechanism as activator of reactive oxygen species generating NADPH oxidase. Reactive Oxygen Species 113-136 Rac family small GTPase 1 Homo sapiens 6-10 19767757-0 2009 CARD9 facilitates microbe-elicited production of reactive oxygen species by regulating the LyGDI-Rac1 complex. Reactive Oxygen Species 49-72 Rac family small GTPase 1 Homo sapiens 97-101 19767757-6 2009 CARD9 associated with the GDP-dissociation inhibitor LyGDI in phagosomes after bacterial and fungal infection and binding of CARD9 suppressed LyGDI-mediated inhibition of the GTPase Rac1, thereby leading to ROS production and bacterial killing in macrophages. Reactive Oxygen Species 207-210 Rac family small GTPase 1 Homo sapiens 182-186 20860838-10 2010 Rac1 activity affects production of ROS, which regulate transformation, metastasis, and oxidative stress. Reactive Oxygen Species 36-39 Rac family small GTPase 1 Homo sapiens 0-4 20860838-11 2010 Protein carbonylation, which is indicative of oxidative stress, was elevated 1.75-fold in p190B transgenic tumors as compared to control tumors suggesting that exogenous p190B expression may affect Rac1-dependent ROS production. Reactive Oxygen Species 213-216 Rac family small GTPase 1 Homo sapiens 198-202 20860838-14 2010 Rac1 activity and oxidative stress are elevated in tumors expressing exogenous p190B suggesting that p190B may promote tumorigenesis through a Rac1/ROS dependent mechanism. Reactive Oxygen Species 148-151 Rac family small GTPase 1 Homo sapiens 0-4 20860838-14 2010 Rac1 activity and oxidative stress are elevated in tumors expressing exogenous p190B suggesting that p190B may promote tumorigenesis through a Rac1/ROS dependent mechanism. Reactive Oxygen Species 148-151 Rac family small GTPase 1 Homo sapiens 143-147 19662499-3 2009 In skeletal muscle cells S1P, through engagement of its S1P(2) receptor, is found to produce a transient burst of reactive oxygen species through a calcium-dependent activation of the small GTPase Rac1. Reactive Oxygen Species 114-137 Rac family small GTPase 1 Homo sapiens 197-201 19633358-7 2009 Knockdown of Rac1 inhibited VEGF-induced ROS production consistent with Rac lying upstream of ROS in this pathway. Reactive Oxygen Species 94-97 Rac family small GTPase 1 Homo sapiens 13-17 19501047-6 2009 Our results also indicate that signaling events downstream of EGFR involved PI3K-dependent activation of Rac1, which mediated the NADPH-generated reactive oxygen species responsible for MMP-9 secretion and activation. Reactive Oxygen Species 146-169 Rac family small GTPase 1 Homo sapiens 105-109 19570918-0 2009 Rac1 modulates stimulus-evoked Ca(2+) release in neuronal growth cones via parallel effects on microtubule/endoplasmic reticulum dynamics and reactive oxygen species production. Reactive Oxygen Species 142-165 Rac family small GTPase 1 Homo sapiens 0-4 19570918-7 2009 The underlying mechanism involves synergistic Rac1 effects on microtubule assembly and reactive oxygen species (ROS) production. Reactive Oxygen Species 87-110 Rac family small GTPase 1 Homo sapiens 46-50 19570918-7 2009 The underlying mechanism involves synergistic Rac1 effects on microtubule assembly and reactive oxygen species (ROS) production. Reactive Oxygen Species 112-115 Rac family small GTPase 1 Homo sapiens 46-50 19570918-8 2009 Rac1 activity modulates Ca(2+) by 1) enhancing microtubule assembly which in turn promotes spread of the ER-based Ca(2+) release machinery into the growth cone periphery, and 2) by increasing ROS production which facilitated inositol 1,4,5-trisphosphate-dependent Ca(2+) release. Reactive Oxygen Species 192-195 Rac family small GTPase 1 Homo sapiens 0-4 19293637-12 2009 We found that HGF modulate Rac-1-regulated ROS production through activation of Akt and ROS regulates uPA production via MAP kinase, which provides a novel clue to clarify the mechanism underlying hepatoma progression. Reactive Oxygen Species 43-46 Rac family small GTPase 1 Homo sapiens 27-32 19328808-5 2009 Cell adhesion and ROS production were inhibited in stimulated THP-1 cells by: inhibition of ROS signaling with N-acetylcysteine, diphenyleneiodonium, or PEG-Catalase; inhibition of PI3Kgamma with siRNA or LY294002; and by Rac1 siRNA. Reactive Oxygen Species 92-95 Rac family small GTPase 1 Homo sapiens 222-226 19322025-9 2009 Both p21-activated kinase and reactive oxygen species played key roles in cytoskeletal reorganization downstream of betaPIX-Rac1. Reactive Oxygen Species 30-53 Rac family small GTPase 1 Homo sapiens 124-128 19429708-3 2009 Small GTPase Rac1, an inflammatory signaling mediator triggering reactive oxygen species (ROS) production by NADPH-oxidases, is implicated in carcinogenesis and tumor angiogenesis. Reactive Oxygen Species 65-88 Rac family small GTPase 1 Homo sapiens 13-17 19429708-3 2009 Small GTPase Rac1, an inflammatory signaling mediator triggering reactive oxygen species (ROS) production by NADPH-oxidases, is implicated in carcinogenesis and tumor angiogenesis. Reactive Oxygen Species 90-93 Rac family small GTPase 1 Homo sapiens 13-17 19293637-6 2009 HGF suppressed the increment in Rac-1-regulated ROS in both cell lines. Reactive Oxygen Species 48-51 Rac family small GTPase 1 Homo sapiens 32-37 19497102-5 2009 We confirmed that Rac-1 regulated ROS production after activation of the AKT pathway with HGF. Reactive Oxygen Species 34-37 Rac family small GTPase 1 Homo sapiens 18-23 19497102-9 2009 CONCLUSION: HGF regulates Rac-1-induced ROS production through the Akt pathway and ROS regulates uPA production and invasion via MAP kinase, which provides novel insight into the mechanisms underlying the progression of gastric cancer. Reactive Oxygen Species 40-43 Rac family small GTPase 1 Homo sapiens 26-31 19344766-4 2009 We demonstrated that, in neuronal cells, TNFalpha and Il-1beta stimulate a transient, redox-dependent reorganization of the actin cytoskeleton into lamellipodia under the regulation of Rac1 and a neuronal NADPH oxidase as the source of ROS. Reactive Oxygen Species 236-239 Rac family small GTPase 1 Homo sapiens 185-189 19366706-0 2009 Phospholipase D-mediated activation of IQGAP1 through Rac1 regulates hyperoxia-induced p47phox translocation and reactive oxygen species generation in lung endothelial cells. Reactive Oxygen Species 113-136 Rac family small GTPase 1 Homo sapiens 54-58 19293637-12 2009 We found that HGF modulate Rac-1-regulated ROS production through activation of Akt and ROS regulates uPA production via MAP kinase, which provides a novel clue to clarify the mechanism underlying hepatoma progression. Reactive Oxygen Species 88-91 Rac family small GTPase 1 Homo sapiens 27-32 19116140-6 2009 Our results also indicate that signaling events downstream of EGF receptor involved PI3K- and Src-dependent activation of Rac1, which mediated the NADPH-generated reactive oxygen species responsible for MMP-2 secretion and activation. Reactive Oxygen Species 163-186 Rac family small GTPase 1 Homo sapiens 122-126 17178255-0 2007 Pitavastatin inhibits lysophosphatidic acid-induced proliferation and monocyte chemoattractant protein-1 expression in aortic smooth muscle cells by suppressing Rac-1-mediated reactive oxygen species generation. Reactive Oxygen Species 176-199 Rac family small GTPase 1 Homo sapiens 161-166 18577517-7 2008 Transfection with dominant negative and constitutive active Rac1 mutants demonstrated that Rac1 was responsible for the increased production of ROS and cell motility by HA. Reactive Oxygen Species 144-147 Rac family small GTPase 1 Homo sapiens 60-64 18577517-7 2008 Transfection with dominant negative and constitutive active Rac1 mutants demonstrated that Rac1 was responsible for the increased production of ROS and cell motility by HA. Reactive Oxygen Species 144-147 Rac family small GTPase 1 Homo sapiens 91-95 18463161-6 2008 We show that c-Src induces Nox1-mediated ROS generation in the HT29 human colon carcinoma cell line through a Rac-dependent mechanism. Reactive Oxygen Species 41-44 Rac family small GTPase 1 Homo sapiens 110-113 18446055-6 2008 Further, we found out that expression of RacN17, a dominant negative mutant of Rac1, suppressed TNF-alpha-induced ROS generation, ICAM-1 expression, and monocyte adhesion to airway epithelium. Reactive Oxygen Species 114-117 Rac family small GTPase 1 Homo sapiens 79-83 18446055-7 2008 These findings suggest that Rac1 lies upstream of ROS generation in the TNF-alpha-induced signaling to ICAM-1 expression in airway epithelium. Reactive Oxygen Species 50-53 Rac family small GTPase 1 Homo sapiens 28-32 18446055-9 2008 Together, we propose that Rac1-ROS-linked cascade mediate TNF-alpha-induced ICAM-1 up-regulation in the airway epithelium via NF-kappaB-dependent manner. Reactive Oxygen Species 31-34 Rac family small GTPase 1 Homo sapiens 26-30 18070887-0 2008 Phosphatidylinositol 3-kinase-dependent membrane recruitment of Rac-1 and p47phox is critical for alpha-platelet-derived growth factor receptor-induced production of reactive oxygen species. Reactive Oxygen Species 166-189 Rac family small GTPase 1 Homo sapiens 64-69 18070887-13 2008 We conclude that PI3K/p110alpha mediates growth factor-dependent ROS production by recruiting p47(phox) and Rac-1 to the cell membrane, thereby assembling the active Nox complex. Reactive Oxygen Species 65-68 Rac family small GTPase 1 Homo sapiens 108-113 17604276-4 2007 Moreover, as shown by the expression of the dominant negative Rac-1 construct, we first report that ox-LDL-mediated cell survival and cell cycle progression depend on Rac-1 GTPase-mediated reactive oxygen species production and on epidermal growth factor receptor transactivation. Reactive Oxygen Species 189-212 Rac family small GTPase 1 Homo sapiens 62-67 17604276-4 2007 Moreover, as shown by the expression of the dominant negative Rac-1 construct, we first report that ox-LDL-mediated cell survival and cell cycle progression depend on Rac-1 GTPase-mediated reactive oxygen species production and on epidermal growth factor receptor transactivation. Reactive Oxygen Species 189-212 Rac family small GTPase 1 Homo sapiens 167-172 17604276-5 2007 By silencing Akt and blocking Erk1/2 MAPK pathways, we also demonstrate that these signals are downstream to Rac-1/reactive oxygen species production and epidermal growth factor receptor activation. Reactive Oxygen Species 115-138 Rac family small GTPase 1 Homo sapiens 109-114 18406051-7 2008 Major source of ROS in ECs is a NADPH oxidase which consists of Nox1, Nox2, Nox4, Nox5, p22phox, p47phox and the small G-protein Rac1. Reactive Oxygen Species 16-19 Rac family small GTPase 1 Homo sapiens 129-133 18259192-4 2008 Here, we demonstrate that reactive oxygen species (ROS) produced through the involvement of the small GTPase Rac-1 upon integrin engagement exert a mandatory role in transducing a pro-survival signal that ensures that cells escape from anoikis. Reactive Oxygen Species 26-49 Rac family small GTPase 1 Homo sapiens 109-114 18259192-4 2008 Here, we demonstrate that reactive oxygen species (ROS) produced through the involvement of the small GTPase Rac-1 upon integrin engagement exert a mandatory role in transducing a pro-survival signal that ensures that cells escape from anoikis. Reactive Oxygen Species 51-54 Rac family small GTPase 1 Homo sapiens 109-114 18305118-8 2008 The signaling implication of reactive oxygen species was examined by comparison with H(2)O(2) and hypoxanthine/xanthine oxidase and by the superoxide dismutase mimetic, MnTMPyP, the Rac1-NAD(P)H oxidase complex inhibitor, apocynin, transfection of a dominant negative Rac1 mutant, and transfection of a p67phox antisense oligonucleotide. Reactive Oxygen Species 29-52 Rac family small GTPase 1 Homo sapiens 182-186 18218673-0 2008 TNF-alpha/cycloheximide-induced apoptosis in intestinal epithelial cells requires Rac1-regulated reactive oxygen species. Reactive Oxygen Species 97-120 Rac family small GTPase 1 Homo sapiens 82-86 18218673-1 2008 Previously we have shown that both Rac1 and c-Jun NH(2)-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-alpha/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive oxygen species (ROS) in apoptosis is unclear. Reactive Oxygen Species 239-262 Rac family small GTPase 1 Homo sapiens 35-39 18218673-1 2008 Previously we have shown that both Rac1 and c-Jun NH(2)-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-alpha/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive oxygen species (ROS) in apoptosis is unclear. Reactive Oxygen Species 264-267 Rac family small GTPase 1 Homo sapiens 35-39 18218673-2 2008 The present studies tested the hypothesis that Rac1-mediated ROS production is involved in TNF-alpha-induced apoptosis. Reactive Oxygen Species 61-64 Rac family small GTPase 1 Homo sapiens 47-51 18218673-4 2008 Inhibition of Rac1 by a specific inhibitor NSC23766 prevented TNF-alpha-induced ROS production. Reactive Oxygen Species 80-83 Rac family small GTPase 1 Homo sapiens 14-18 18218673-7 2008 Inhibition of Rac1 by expression of dominant negative Rac1 decreased TNF-alpha-induced mitochondrial ROS production. Reactive Oxygen Species 101-104 Rac family small GTPase 1 Homo sapiens 14-18 18218673-7 2008 Inhibition of Rac1 by expression of dominant negative Rac1 decreased TNF-alpha-induced mitochondrial ROS production. Reactive Oxygen Species 101-104 Rac family small GTPase 1 Homo sapiens 54-58 18218673-8 2008 Moreover, TNF-alpha-induced cytosolic ROS production was inhibited by Rac1 inhibition, diphenyleneiodonium (DPI, an inhibitor of NADPH oxidase), and NAC. Reactive Oxygen Species 38-41 Rac family small GTPase 1 Homo sapiens 70-74 18218673-12 2008 Thus these results indicate that TNF-alpha-induced apoptosis requires Rac1-dependent ROS production in intestinal epithelial cells. Reactive Oxygen Species 85-88 Rac family small GTPase 1 Homo sapiens 70-74 18192505-5 2008 Increased ROS levels appear to be produced via STAT5 signaling and activation of RAC1, an essential component of ROS-producing NADPH oxidases. Reactive Oxygen Species 10-13 Rac family small GTPase 1 Homo sapiens 81-85 18192505-5 2008 Increased ROS levels appear to be produced via STAT5 signaling and activation of RAC1, an essential component of ROS-producing NADPH oxidases. Reactive Oxygen Species 113-116 Rac family small GTPase 1 Homo sapiens 81-85 18192505-6 2008 A direct association of RAC1-GTP binding to phosphorylated STAT5 (pSTAT5) provides a possible mechanism for ROS generation. Reactive Oxygen Species 108-111 Rac family small GTPase 1 Homo sapiens 24-28 18292530-7 2008 NADPH oxidase is a key source of ROS generation induced by FasL, and its inhibition by dominant-negative Rac1 expression or by chemical inhibitor decreased the cell death response to FasL. Reactive Oxygen Species 33-36 Rac family small GTPase 1 Homo sapiens 105-109 18047620-14 2008 In addition, Rac1-induced cardiomyocyte hypertrophy is mediated by the generation of ROS. Reactive Oxygen Species 85-88 Rac family small GTPase 1 Homo sapiens 13-17 17854274-3 2007 We hypothesized that reactive oxygen species produced by NADPH oxidase may autoregulate the complex by inhibiting Rac activity. Reactive Oxygen Species 21-44 Rac family small GTPase 1 Homo sapiens 114-117 17659204-3 2007 We hypothesized that activation of Rac1 GTPase contributes to the pathogenesis of AF via activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and production of reactive oxygen species. Reactive Oxygen Species 181-204 Rac family small GTPase 1 Homo sapiens 35-39 17178255-10 2007 These results suggest that pitavastatin could block the LPA-induced proliferation and MCP-1 expression in SMCs by suppressing Rac-1-mediated NADPH oxidase-dependent ROS generation. Reactive Oxygen Species 165-168 Rac family small GTPase 1 Homo sapiens 126-131 17178255-7 2007 Furthermore, overexpression of dominant negative Rac-1 mutant was found to inhibit the LPA-induced ROS generation in SMCs. Reactive Oxygen Species 99-102 Rac family small GTPase 1 Homo sapiens 49-54 17318182-4 2007 CCN1 acts through binding to integrins alpha(v)beta(5), alpha(6)beta(1), and syndecan-4, triggering the generation of reactive oxygen species (ROS) through a Rac1-dependent mechanism via 5-lipoxygenase and the mitochondria, leading to the biphasic activation of JNK necessary for apoptosis. Reactive Oxygen Species 118-141 Rac family small GTPase 1 Homo sapiens 158-162 17318182-4 2007 CCN1 acts through binding to integrins alpha(v)beta(5), alpha(6)beta(1), and syndecan-4, triggering the generation of reactive oxygen species (ROS) through a Rac1-dependent mechanism via 5-lipoxygenase and the mitochondria, leading to the biphasic activation of JNK necessary for apoptosis. Reactive Oxygen Species 143-146 Rac family small GTPase 1 Homo sapiens 158-162 16926363-4 2006 NADPH (nicotinamide adenine dinucleotide phosphate) oxidase is one of the major sources of ROS in vasculature; it consists of a catalytic subunit (Nox1, Nox2, Nox3, Nox4, or Nox5), p22phox, p47phox, p67phox, and the small guanosine triphosphatase Rac1. Reactive Oxygen Species 91-94 Rac family small GTPase 1 Homo sapiens 247-251 17204833-1 2007 BACKGROUND: Rac1 is a Rho-family small GTP-ase, when activated is pivotal in NAD(P)H oxidase (NOX) activation and generation of reactive oxygen species (ROS). Reactive Oxygen Species 128-151 Rac family small GTPase 1 Homo sapiens 12-16 17204833-1 2007 BACKGROUND: Rac1 is a Rho-family small GTP-ase, when activated is pivotal in NAD(P)H oxidase (NOX) activation and generation of reactive oxygen species (ROS). Reactive Oxygen Species 153-156 Rac family small GTPase 1 Homo sapiens 12-16 17204833-3 2007 Thus in states of albumin overload, Rac1 activation could lead to NOX activation and ROS formation in the PTC. Reactive Oxygen Species 85-88 Rac family small GTPase 1 Homo sapiens 36-40 17015444-3 2006 An analysis of their relationship revealed that the mitochondria respond to serum withdrawal within a few minutes, and the ROS produced by the mitochondria trigger Nox1 action by stimulating phosphoinositide 3-kinase (PI3K) and Rac1. Reactive Oxygen Species 123-126 Rac family small GTPase 1 Homo sapiens 228-232 17015444-5 2006 Functional analysis suggested that, although the mitochondria contribute to the early (0-4 h) accumulation of ROS, the maintenance of the induced ROS levels to the later (4-8 h) phase required the action of the PI3K/Rac1/Nox1 pathway. Reactive Oxygen Species 146-149 Rac family small GTPase 1 Homo sapiens 216-220 17008589-4 2006 The increase was regulated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (including the activation of subunits p47(phox) and Rac1), which mediates the production of reactive oxygen species and the activation of intracellular mitogen-activated protein kinase signaling pathways. Reactive Oxygen Species 182-205 Rac family small GTPase 1 Homo sapiens 142-146 16551621-4 2006 Consistent with data from other cell types we demonstrate that both Rac1 and Rac1b stimulate transcriptional activation from reporter genes driven by NF-kappaB motifs or the cyclin D1 promoter in an IkappaBalpha- and reactive oxygen species-dependent manner. Reactive Oxygen Species 217-240 Rac family small GTPase 1 Homo sapiens 68-72 16636067-1 2006 Rac1 has been implicated in the generation of reactive oxygen species (ROS) in several cell types, but the enzymatic origin of the ROS has not been proven. Reactive Oxygen Species 46-69 Rac family small GTPase 1 Homo sapiens 0-4 16636067-1 2006 Rac1 has been implicated in the generation of reactive oxygen species (ROS) in several cell types, but the enzymatic origin of the ROS has not been proven. Reactive Oxygen Species 71-74 Rac family small GTPase 1 Homo sapiens 0-4 16636067-1 2006 Rac1 has been implicated in the generation of reactive oxygen species (ROS) in several cell types, but the enzymatic origin of the ROS has not been proven. Reactive Oxygen Species 131-134 Rac family small GTPase 1 Homo sapiens 0-4 16636067-5 2006 Decreased Rac1 expression using small interfering RNA reduced Nox1-dependent ROS. Reactive Oxygen Species 77-80 Rac family small GTPase 1 Homo sapiens 10-14 16636067-12 2006 A model is presented comparing activation by regulatory subunits of Nox1 versus gp91(phox) (Nox2) in which Rac1 activation provides a major trigger that acutely activates Nox1-dependent ROS generation. Reactive Oxygen Species 186-189 Rac family small GTPase 1 Homo sapiens 107-111 16781692-5 2006 The major source of ROS in EC is a NADPH oxidase which consists of Nox1, Nox2 (gp91phox), Nox4, p22phox, p47phox, p67phox and the small G protein Rac1. Reactive Oxygen Species 20-23 Rac family small GTPase 1 Homo sapiens 146-150 16782079-4 2006 An important source of ROS within EC is the non-phagocytic NAD(P)H oxidase, and the small GTPase Rac1 plays a central role in activating this complex. Reactive Oxygen Species 23-26 Rac family small GTPase 1 Homo sapiens 97-101 16514078-2 2006 The family of NADPH oxidases (NOXes) plays an important role in the production of ROS in response to receptor agonists such as growth factors or inflammatory cytokines that signal through the Rho-like small GTPases Rac1 or Rac2. Reactive Oxygen Species 82-85 Rac family small GTPase 1 Homo sapiens 215-219 16251354-1 2006 The rac1 GTPase and the p66shc adaptor protein regulate intracellular levels of reactive oxygen species (ROS). Reactive Oxygen Species 80-103 Rac family small GTPase 1 Homo sapiens 4-8 16251354-1 2006 The rac1 GTPase and the p66shc adaptor protein regulate intracellular levels of reactive oxygen species (ROS). Reactive Oxygen Species 105-108 Rac family small GTPase 1 Homo sapiens 4-8 16049136-3 2005 ROS production was attenuated by preincubation with a peptide (gp91ds-tat) that inhibits the association of the gp91(phox) subunit with the p47(phox) subunit of NADPH oxidase and by the expression of a dominant-negative form of Rac-1 (Rac1N17). Reactive Oxygen Species 0-3 Rac family small GTPase 1 Homo sapiens 228-233 16298859-0 2005 Rac1-NADPH oxidase-regulated generation of reactive oxygen species mediates glutamate-induced apoptosis in SH-SY5Y human neuroblastoma cells. Reactive Oxygen Species 43-66 Rac family small GTPase 1 Homo sapiens 0-4 16298859-6 2005 Moreover, the expression of Rac1N17, a dominant negative mutant of Rac1, significantly blocked the glutamate-induced ROS generation and cell death. Reactive Oxygen Species 117-120 Rac family small GTPase 1 Homo sapiens 28-32 16049136-3 2005 ROS production was attenuated by preincubation with a peptide (gp91ds-tat) that inhibits the association of the gp91(phox) subunit with the p47(phox) subunit of NADPH oxidase and by the expression of a dominant-negative form of Rac-1 (Rac1N17). Reactive Oxygen Species 0-3 Rac family small GTPase 1 Homo sapiens 235-242 16049136-4 2005 These results suggest that ROS production in response to Ang-1 exposure originates mainly from a Rac-1-dependent NADPH oxidase. Reactive Oxygen Species 27-30 Rac family small GTPase 1 Homo sapiens 97-102 15976327-2 2005 These effects are mediated through the Ang II type 1 receptor (AT1R) and require its trafficking through caveolin-1 (Cav1)-enriched lipid rafts and reactive oxygen species (ROS) derived from Rac1-dependent NAD(P)H oxidase. Reactive Oxygen Species 148-171 Rac family small GTPase 1 Homo sapiens 191-195 16051607-8 2005 Like Rac1-T17N, the NADPH oxidase inhibitor diphenylene iodonium and the tyrosine kinase inhibitor herbimycin A blocked TGF-beta-induced p38 activation and BGN expression, suggesting that Rac1 exerts its effect on BGN and p38 through increasing NADPH oxidase activity and subsequent production of reactive oxygen species. Reactive Oxygen Species 297-320 Rac family small GTPase 1 Homo sapiens 188-192 15976327-10 2005 CONCLUSIONS: Cav1 plays an essential role in AT1R targeting into Cav1-enriched lipid rafts and Rac1 activation, which are required for proper organization of ROS-dependent Ang II signaling linked to VSMC hypertrophy. Reactive Oxygen Species 158-161 Rac family small GTPase 1 Homo sapiens 95-99 15976327-2 2005 These effects are mediated through the Ang II type 1 receptor (AT1R) and require its trafficking through caveolin-1 (Cav1)-enriched lipid rafts and reactive oxygen species (ROS) derived from Rac1-dependent NAD(P)H oxidase. Reactive Oxygen Species 173-176 Rac family small GTPase 1 Homo sapiens 191-195 15861318-4 2004 Because Rac1 is a requisite component of NADPH oxidase, which is a major source of reactive oxygen species in cardiovascular cells, the ability of statins to inhibit Rac1-mediated oxidative stress contributes importantly to their inhibitory effects on cardiac hypertrophy. Reactive Oxygen Species 83-106 Rac family small GTPase 1 Homo sapiens 8-12 15817678-2 2005 Here, we show RANKL stimulation of BMM cells transiently increased the intracellular level of reactive oxygen species (ROS) through a signaling cascade involving TNF (tumor necrosis factor) receptor-associated factor (TRAF) 6, Rac1, and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (Nox) 1. Reactive Oxygen Species 94-117 Rac family small GTPase 1 Homo sapiens 227-231 15377495-0 2004 Important role for Rac1 in regulating reactive oxygen species generation and pulmonary arterial smooth muscle cell growth. Reactive Oxygen Species 38-61 Rac family small GTPase 1 Homo sapiens 19-23 15377495-4 2004 Here we demonstrate that ROS generation in ovine pulmonary arterial smooth muscle cells (PASMCs) requires the activation of Rac1, implicating this protein as an important subunit of the NADPH oxidase complex. Reactive Oxygen Species 25-28 Rac family small GTPase 1 Homo sapiens 124-128 15377495-7 2004 The inhibition of Rac1 by GGTI-287 led us to more specifically target Rac1 to investigate its role in the generation of ROS and cellular proliferation. Reactive Oxygen Species 120-123 Rac family small GTPase 1 Homo sapiens 70-74 15377495-13 2004 These results indicate the importance of Rac1 in ROS generation and proliferation of vascular smooth muscle cells. Reactive Oxygen Species 49-52 Rac family small GTPase 1 Homo sapiens 41-45 16099726-1 2005 Both in vivo models of ischemia/reperfusion and in vitro models of hypoxia (H)/reoxygenation (R) have demonstrated the crucial role of the Rac1-regulated NADPH oxidase in the production of injurious reactive oxygen species (ROS) by vascular endothelial cells (ECs). Reactive Oxygen Species 199-222 Rac family small GTPase 1 Homo sapiens 139-143 16099726-1 2005 Both in vivo models of ischemia/reperfusion and in vitro models of hypoxia (H)/reoxygenation (R) have demonstrated the crucial role of the Rac1-regulated NADPH oxidase in the production of injurious reactive oxygen species (ROS) by vascular endothelial cells (ECs). Reactive Oxygen Species 224-227 Rac family small GTPase 1 Homo sapiens 139-143 16099726-9 2005 In conclusion, ROS generated via the Rac1-dependent pathway are major contributors to the H/R-induced lipid peroxidation in HUVECs, and ND is able to induce Rac1-dependent ROS production and lipid peroxidation of at least the same magnitude as H/R. Reactive Oxygen Species 15-18 Rac family small GTPase 1 Homo sapiens 37-41 16099726-9 2005 In conclusion, ROS generated via the Rac1-dependent pathway are major contributors to the H/R-induced lipid peroxidation in HUVECs, and ND is able to induce Rac1-dependent ROS production and lipid peroxidation of at least the same magnitude as H/R. Reactive Oxygen Species 172-175 Rac family small GTPase 1 Homo sapiens 157-161 15817678-2 2005 Here, we show RANKL stimulation of BMM cells transiently increased the intracellular level of reactive oxygen species (ROS) through a signaling cascade involving TNF (tumor necrosis factor) receptor-associated factor (TRAF) 6, Rac1, and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (Nox) 1. Reactive Oxygen Species 119-122 Rac family small GTPase 1 Homo sapiens 227-231 15778498-8 2005 These results implicate Pyk2 in the reduced cell-cell adhesion induced by the Rac-mediated production of ROS through the tyrosine phosphorylation of beta-catenin. Reactive Oxygen Species 105-108 Rac family small GTPase 1 Homo sapiens 78-81 15706084-4 2005 Third, it controls the intracellular reactive oxygen species production by negatively regulating the activity of the Ras-related GTPase Rac1. Reactive Oxygen Species 37-60 Rac family small GTPase 1 Homo sapiens 136-140 15861318-4 2004 Because Rac1 is a requisite component of NADPH oxidase, which is a major source of reactive oxygen species in cardiovascular cells, the ability of statins to inhibit Rac1-mediated oxidative stress contributes importantly to their inhibitory effects on cardiac hypertrophy. Reactive Oxygen Species 83-106 Rac family small GTPase 1 Homo sapiens 166-170 15142861-7 2004 CONCLUSIONS: These results suggest that proper Rac1 and AT1R trafficking into caveolae/lipid rafts requires the integrity of microtubules and provide insight into the essential role of microtubules for the spatial-temporal organization of ROS-dependent and caveolae/lipid rafts-dependent AT(1)R signaling linked to vascular hypertrophy. Reactive Oxygen Species 239-242 Rac family small GTPase 1 Homo sapiens 47-51 15544038-7 2004 Importantly, the major source of ROS in EC is a NAD(P)H oxidase and EC express all the components of phagocytic NAD(P)H oxidase including gp91phox, p22phox, p47phox, p67phox and the small G protein Rac1. Reactive Oxygen Species 33-36 Rac family small GTPase 1 Homo sapiens 198-202 15361285-9 2004 We also confirmed that rac1 was located upstream of ROS in the WPB release pathway. Reactive Oxygen Species 52-55 Rac family small GTPase 1 Homo sapiens 23-27 15361285-10 2004 CONCLUSIONS: Small G-protein rac1 medicates ligand-induced release of Weibel-Palade Bodies in human aortic endothelial cells, and the signal pathway of WPB release is a rac1-dependent ROS regulating mechanism. Reactive Oxygen Species 184-187 Rac family small GTPase 1 Homo sapiens 29-33 15361285-10 2004 CONCLUSIONS: Small G-protein rac1 medicates ligand-induced release of Weibel-Palade Bodies in human aortic endothelial cells, and the signal pathway of WPB release is a rac1-dependent ROS regulating mechanism. Reactive Oxygen Species 184-187 Rac family small GTPase 1 Homo sapiens 169-173 15238820-5 2004 Since Rac1 is a requisite component of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which is a major source of reactive oxygen species (ROS) in cardiovascular cells, the ability of statins to inhibit Rac1-mediated oxidative stress makes an important contribution to their inhibitory effects on cardiac hypertrophy. Reactive Oxygen Species 135-158 Rac family small GTPase 1 Homo sapiens 6-10 15238820-5 2004 Since Rac1 is a requisite component of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which is a major source of reactive oxygen species (ROS) in cardiovascular cells, the ability of statins to inhibit Rac1-mediated oxidative stress makes an important contribution to their inhibitory effects on cardiac hypertrophy. Reactive Oxygen Species 160-163 Rac family small GTPase 1 Homo sapiens 6-10 15123662-6 2004 Cdc42 acted as a competitive inhibitor of Rac1- and Rac2-mediated ROS formation in a recombinant cell-free oxidase system. Reactive Oxygen Species 66-69 Rac family small GTPase 1 Homo sapiens 42-46 15123662-8 2004 Transient expression of Cdc42Q61L inhibited ROS formation induced by constitutively active Rac1 in an NADPH oxidase-expressing Cos7 cell line. Reactive Oxygen Species 44-47 Rac family small GTPase 1 Homo sapiens 91-95 15121857-6 2004 These results suggest that ROS production in growth factor-stimulated cells is mediated by the sequential activation of PI3K, beta Pix, and Rac1, which then binds to Nox1 to stimulate its NADPH oxidase activity. Reactive Oxygen Species 27-30 Rac family small GTPase 1 Homo sapiens 140-144 15521546-4 2004 Because Rac1 is a requisite component of reduced nicotinamide adenine dinucleotide phosphate oxidase, which is a major source of reactive oxygen species in cardiovascular cells, the ability of statins to inhibit Rac1-mediated oxidative stress contributes importantly to their inhibitory effects on cardiac hypertrophy. Reactive Oxygen Species 129-152 Rac family small GTPase 1 Homo sapiens 8-12 15158121-9 2004 These findings suggest that the signal transduction pathway leading to hypertrophy involves Ca(2+)-induced Pyk2 activation followed by Rac1-dependent ROS production. Reactive Oxygen Species 150-153 Rac family small GTPase 1 Homo sapiens 135-139 12861025-9 2003 These results identify Rac-induced ROS as a new pathway involved in the regulation of TSP2 expression. Reactive Oxygen Species 35-38 Rac family small GTPase 1 Homo sapiens 23-26 15124904-5 2004 GA-induced ROS production was also inhibited in RacN17 cell line overexpressing a dominant negative mutant of Rac1. Reactive Oxygen Species 11-14 Rac family small GTPase 1 Homo sapiens 110-114 15124904-6 2004 Furthermore, GA treatment induces MAPKs activation (SAPK/JNK and p38) and Hsp70 expression in ROS dependent manner, suggesting that GA turns on the signaling pathway by generation of ROS through Rac1. Reactive Oxygen Species 94-97 Rac family small GTPase 1 Homo sapiens 195-199 15124904-6 2004 Furthermore, GA treatment induces MAPKs activation (SAPK/JNK and p38) and Hsp70 expression in ROS dependent manner, suggesting that GA turns on the signaling pathway by generation of ROS through Rac1. Reactive Oxygen Species 183-186 Rac family small GTPase 1 Homo sapiens 195-199 12963641-2 2003 A potential source of myocardial ROS is the NADPH oxidase, which is regulated by the small GTP-binding protein rac1. Reactive Oxygen Species 33-36 Rac family small GTPase 1 Homo sapiens 111-115 14512443-0 2003 G Protein betagamma subunits stimulate p114RhoGEF, a guanine nucleotide exchange factor for RhoA and Rac1: regulation of cell shape and reactive oxygen species production. Reactive Oxygen Species 136-159 Rac family small GTPase 1 Homo sapiens 101-105 14512443-11 2003 Functional significance of Rac1 activation was established by the ability of p114RhoGEF to induce production of reactive oxygen species (ROS) followed by activation of NADPH oxidase enzyme complex. Reactive Oxygen Species 112-135 Rac family small GTPase 1 Homo sapiens 27-31 14512443-11 2003 Functional significance of Rac1 activation was established by the ability of p114RhoGEF to induce production of reactive oxygen species (ROS) followed by activation of NADPH oxidase enzyme complex. Reactive Oxygen Species 137-140 Rac family small GTPase 1 Homo sapiens 27-31 12842860-6 2003 Dominant negative Rac1 (N17Rac1) as well as AS Nox4 inhibited ROS generation in response to ANG II and AA, whereas constitutively active Rac1 stimulated ROS formation. Reactive Oxygen Species 62-65 Rac family small GTPase 1 Homo sapiens 18-22 12842860-10 2003 These data provide the first evidence that activation by AA of a Rac1-regulated, Nox4-based NAD(P)H oxidase and subsequent generation of ROS mediate the effect of ANG II on Akt/PKB activation and protein synthesis in MCs. Reactive Oxygen Species 137-140 Rac family small GTPase 1 Homo sapiens 65-69 12728249-1 2003 Rac1-regulated reactive oxygen species (ROS) production has been implicated in apoptosis. Reactive Oxygen Species 15-38 Rac family small GTPase 1 Homo sapiens 0-4 12728249-1 2003 Rac1-regulated reactive oxygen species (ROS) production has been implicated in apoptosis. Reactive Oxygen Species 40-43 Rac family small GTPase 1 Homo sapiens 0-4 12493759-1 2003 Rac1 GTPase is essential for the activation of the NAD(P)H oxidase complex and, thereby, regulates the release of reactive oxygen species (ROS) in the vessel wall. Reactive Oxygen Species 114-137 Rac family small GTPase 1 Homo sapiens 0-4 12719791-4 2003 We therefore investigated the role of the GTPase Rac1 which modulates ROS production in the pathway leading to HIF-1 and PAI-1 induction. Reactive Oxygen Species 70-73 Rac family small GTPase 1 Homo sapiens 49-53 12719791-5 2003 Overexpression of constitutively activated (RacG12V) or dominant-negative (RacT17N) Rac1 increased or decreased, respectively, ROS production. Reactive Oxygen Species 127-130 Rac family small GTPase 1 Homo sapiens 84-88 12493759-1 2003 Rac1 GTPase is essential for the activation of the NAD(P)H oxidase complex and, thereby, regulates the release of reactive oxygen species (ROS) in the vessel wall. Reactive Oxygen Species 139-142 Rac family small GTPase 1 Homo sapiens 0-4 14572163-8 2003 Rac1 also regulates NADPH oxidase, which is a major source of reactive oxygen species (ROS) in cardiovascular cells. Reactive Oxygen Species 62-85 Rac family small GTPase 1 Homo sapiens 0-4 12556491-3 2003 Here we show that GPCR-stimulated Rac activity and the subsequent generation of reactive oxygen species are necessary for activating tyrosine phosphorylation of Jaks and STAT-dependent transcription. Reactive Oxygen Species 80-103 Rac family small GTPase 1 Homo sapiens 34-37 12566069-5 2003 The presence of ROS scavengers and an inhibitor of NADPH oxidase or expression of a dominant negative form of Rac1 blocks ROS production, deltapsi(m) collapse, and the subsequent activation of caspases. Reactive Oxygen Species 122-125 Rac family small GTPase 1 Homo sapiens 110-114 12566069-6 2003 These observations indicate that NaSal mediates ROS production critical in the triggering of apoptotic tumor cell death through a Rac1-NADPH oxidase-dependent pathway. Reactive Oxygen Species 48-51 Rac family small GTPase 1 Homo sapiens 130-134 14572163-8 2003 Rac1 also regulates NADPH oxidase, which is a major source of reactive oxygen species (ROS) in cardiovascular cells. Reactive Oxygen Species 87-90 Rac family small GTPase 1 Homo sapiens 0-4 14572163-9 2003 Growing evidence suggests that ROS may be involved in the process of cardiac hypertrophy and recent research has shown that statins attenuate oxidative stress through inhibition of Rac1. Reactive Oxygen Species 31-34 Rac family small GTPase 1 Homo sapiens 181-185 11735132-9 2001 These results suggest that mechanical stress induces cardiac hypertrophy through the Rac1-ROS-p38MAPK pathway in cardiac myocytes. Reactive Oxygen Species 90-93 Rac family small GTPase 1 Homo sapiens 85-89 12058277-1 2002 The rac1 GTPase promotes oxidative stress through reactive oxygen species (ROS) production, whereas the DNA repair enzyme and transcriptional regulator redox factor-1 (ref-1) protects against cell death due to oxidative stimuli. Reactive Oxygen Species 50-73 Rac family small GTPase 1 Homo sapiens 4-8 12058277-1 2002 The rac1 GTPase promotes oxidative stress through reactive oxygen species (ROS) production, whereas the DNA repair enzyme and transcriptional regulator redox factor-1 (ref-1) protects against cell death due to oxidative stimuli. Reactive Oxygen Species 75-78 Rac family small GTPase 1 Homo sapiens 4-8 11735132-7 2001 Mechanical stretch increased intracellular ROS generation, which was abrogated by overexpression of D.N.Rac1 and attenuated by overexpression of D.N.RhoA and D.N.Cdc42. Reactive Oxygen Species 43-46 Rac family small GTPase 1 Homo sapiens 104-108 12038964-0 2002 Implication of the small GTPase Rac1 in the generation of reactive oxygen species in response to beta-amyloid in C6 astroglioma cells. Reactive Oxygen Species 58-81 Rac family small GTPase 1 Homo sapiens 32-36 12038964-2 2002 Subsequent characterization of the signalling pathway revealed that expression of RacN17, a dominant-negative Rac1 mutant, completely blocked Abeta(25-35)-induced generation of ROS, which is indicative of the crucial role played by Rac GTPase in this process. Reactive Oxygen Species 177-180 Rac family small GTPase 1 Homo sapiens 110-114 12055077-5 2002 Either EC treatment with the antioxidant pyrrolidine dithiocarbamate (PDTC) or infection with AdRac1N17, which results in expression of the dominant-negative form of Rac1, abolished H/RO-induced ROS production, attenuated rolling, and abolished stable adhesion of U937 cells to H/RO-exposed ECs. Reactive Oxygen Species 195-198 Rac family small GTPase 1 Homo sapiens 96-100 12055077-8 2002 We concluded that the Rac1-dependent ROS partially regulate rolling and exclusively regulate stable adhesion of monocytic cells to ECs after H/RO and that stable adhesion, but not rolling, is mediated by ROS-induced expression of VCAM-1. Reactive Oxygen Species 37-40 Rac family small GTPase 1 Homo sapiens 22-26 12055077-8 2002 We concluded that the Rac1-dependent ROS partially regulate rolling and exclusively regulate stable adhesion of monocytic cells to ECs after H/RO and that stable adhesion, but not rolling, is mediated by ROS-induced expression of VCAM-1. Reactive Oxygen Species 204-207 Rac family small GTPase 1 Homo sapiens 22-26 12058277-7 2002 We conclude that inhibition of oxidative stress is another mechanism by which ref-1 protects against apoptosis, and that this is achieved through modulation of cytoplasmic rac1-regulated ROS generation. Reactive Oxygen Species 187-190 Rac family small GTPase 1 Homo sapiens 172-176 11585836-2 2001 We evaluated the impact of Rac1-induced reactive oxygen species production on the turnover of Rac1 itself in human aortic endothelial cells. Reactive Oxygen Species 40-63 Rac family small GTPase 1 Homo sapiens 27-31 11585836-2 2001 We evaluated the impact of Rac1-induced reactive oxygen species production on the turnover of Rac1 itself in human aortic endothelial cells. Reactive Oxygen Species 40-63 Rac family small GTPase 1 Homo sapiens 94-98 11494050-0 2001 TGF-beta-induced p38 activation is mediated by Rac1-regulated generation of reactive oxygen species in cultured human keratinocytes. Reactive Oxygen Species 76-99 Rac family small GTPase 1 Homo sapiens 47-51 11494050-13 2001 Collectively, our data suggest that TGF-beta-induced p38 activation is mediated by Rac1-regulated generation of reactive oxygen species in cultured human keratinocytes. Reactive Oxygen Species 112-135 Rac family small GTPase 1 Homo sapiens 83-87 10934206-3 2000 Consistent with the role of Rac in that process, stable expression of Rac(Asn-17), a dominant negative Rac1 mutant, completely blocked TNF-alpha-induced ROS generation. Reactive Oxygen Species 153-156 Rac family small GTPase 1 Homo sapiens 103-107 10952983-2 2000 We show that the small GTPase rac1, and Rac1-regulated reactive oxygen species (ROS) play an important role in stress-stimulated heat shock response. Reactive Oxygen Species 55-78 Rac family small GTPase 1 Homo sapiens 40-44 10952983-2 2000 We show that the small GTPase rac1, and Rac1-regulated reactive oxygen species (ROS) play an important role in stress-stimulated heat shock response. Reactive Oxygen Species 80-83 Rac family small GTPase 1 Homo sapiens 40-44 10952983-7 2000 These results show that Rac1 is a necessary but insufficient component of the stress-induced signaling pathway that leads to ROS production, activation of HSFs, and transcription of heat shock proteins. Reactive Oxygen Species 125-128 Rac family small GTPase 1 Homo sapiens 24-28 11402028-0 2001 Lipopolysaccharide induces Rac1-dependent reactive oxygen species formation and coordinates tumor necrosis factor-alpha secretion through IKK regulation of NF-kappa B. Reactive Oxygen Species 42-65 Rac family small GTPase 1 Homo sapiens 27-31 11402028-4 2001 The present study demonstrates for the first time that the activation of Rac1 (a GTP-binding protein), and the subsequent production of ROS, constitutes a major pathway involved in NFkappaB-mediated tumor necrosis factor-alpha (TNFalpha) secretion following LPS challenge in macrophages. Reactive Oxygen Species 136-139 Rac family small GTPase 1 Homo sapiens 73-77 11402028-5 2001 Expression of a dominant negative mutant of Rac1 (N17Rac1) reduced Rac1 activation, ROS formation, NFkappaB activation, and TNFalpha secretion following LPS stimulation. Reactive Oxygen Species 84-87 Rac family small GTPase 1 Homo sapiens 44-48 11402028-5 2001 Expression of a dominant negative mutant of Rac1 (N17Rac1) reduced Rac1 activation, ROS formation, NFkappaB activation, and TNFalpha secretion following LPS stimulation. Reactive Oxygen Species 84-87 Rac family small GTPase 1 Homo sapiens 53-57 10973919-10 2000 These findings show that Rac1 is an important regulator of TNF-induced ROS production in endothelial cells. Reactive Oxygen Species 71-74 Rac family small GTPase 1 Homo sapiens 25-29 10973919-11 2000 Moreover, they suggest that Rac1-dependent ROS, directly or indirectly, lead to protection against TNF-induced death, whereas mitochondrial-derived ROS promote TNF-induced apoptosis. Reactive Oxygen Species 43-46 Rac family small GTPase 1 Homo sapiens 28-32 10973919-0 2000 Rac1 inhibits TNF-alpha-induced endothelial cell apoptosis: dual regulation by reactive oxygen species. Reactive Oxygen Species 79-102 Rac family small GTPase 1 Homo sapiens 0-4 10973919-5 2000 Adenoviral-mediated gene transfer of a dominant negative form of the small GTPase Rac1 (Rac1N17) partially suppressed the TNF-induced oxidative burst without affecting TNF-induced mitochondrial ROS production. Reactive Oxygen Species 194-197 Rac family small GTPase 1 Homo sapiens 82-86 9705280-1 1998 The Rho family GTPases, Rac1 and Rac2, regulate a variety of cellular functions including cytoskeletal reorganization, the generation of reactive oxygen species, G1 cell cycle progression and, in concert with Ras, oncogenic transformation. Reactive Oxygen Species 137-160 Rac family small GTPase 1 Homo sapiens 24-28 9576845-2 1998 The dominant-negative mutant hRac1(T17N) inhibits the NADH-stimulated production of ROS in HepG2 cells, whereas the constitutively activated hRac1(G12V) leads to an increase in intracellular ROS concentration. Reactive Oxygen Species 84-87 Rac family small GTPase 1 Homo sapiens 29-34 9576845-2 1998 The dominant-negative mutant hRac1(T17N) inhibits the NADH-stimulated production of ROS in HepG2 cells, whereas the constitutively activated hRac1(G12V) leads to an increase in intracellular ROS concentration. Reactive Oxygen Species 191-194 Rac family small GTPase 1 Homo sapiens 29-34 9576845-2 1998 The dominant-negative mutant hRac1(T17N) inhibits the NADH-stimulated production of ROS in HepG2 cells, whereas the constitutively activated hRac1(G12V) leads to an increase in intracellular ROS concentration. Reactive Oxygen Species 191-194 Rac family small GTPase 1 Homo sapiens 141-146 9576845-4 1998 These results demonstrate that hRac1, and not hRac2, is involved in the regulation of ROS production in HepG2 cells and suggest that hRac1 specifically functions in the non-phagocytic NAD(P)H oxidase complex. Reactive Oxygen Species 86-89 Rac family small GTPase 1 Homo sapiens 31-36 9576845-4 1998 These results demonstrate that hRac1, and not hRac2, is involved in the regulation of ROS production in HepG2 cells and suggest that hRac1 specifically functions in the non-phagocytic NAD(P)H oxidase complex. Reactive Oxygen Species 86-89 Rac family small GTPase 1 Homo sapiens 133-138 8943367-7 1996 In an effort to further explore how rac proteins might regulate NF-kappaB activity, we demonstrate that expression of V12rac1 in HeLa cells or stimulation with cytokine results in a significant increase in intracellular reactive oxygen species (ROS). Reactive Oxygen Species 220-243 Rac family small GTPase 1 Homo sapiens 36-39 8943367-7 1996 In an effort to further explore how rac proteins might regulate NF-kappaB activity, we demonstrate that expression of V12rac1 in HeLa cells or stimulation with cytokine results in a significant increase in intracellular reactive oxygen species (ROS). Reactive Oxygen Species 245-248 Rac family small GTPase 1 Homo sapiens 36-39 8943367-9 1996 These results suggest that in HeLa cells, rac1 regulates intracellular ROS production and that rac proteins function as part of a redox-dependent signal transduction pathway leading to NF-kappaB activation. Reactive Oxygen Species 71-74 Rac family small GTPase 1 Homo sapiens 42-46 8943367-9 1996 These results suggest that in HeLa cells, rac1 regulates intracellular ROS production and that rac proteins function as part of a redox-dependent signal transduction pathway leading to NF-kappaB activation. Reactive Oxygen Species 71-74 Rac family small GTPase 1 Homo sapiens 42-45 34597669-6 2021 Global transcriptomic, biochemical, and cellular analyses indicated that GCN2 is necessary for maintenance of intracellular free amino acids, particularly cysteine, as well as coordination of RAC1-GTP-driven reactive oxygen species (ROS) generation, lamellipodia formation, and focal adhesion dynamics following keratinocyte wounding. Reactive Oxygen Species 208-231 Rac family small GTPase 1 Homo sapiens 192-196 34064109-4 2021 Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity. Reactive Oxygen Species 56-59 Rac family small GTPase 1 Homo sapiens 257-261 34064109-4 2021 Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity. Reactive Oxygen Species 77-80 Rac family small GTPase 1 Homo sapiens 257-261 9576744-1 1998 We demonstrate that adenoviral-mediated gene transfer of a dominant negative rac1 gene product (N17rac1) inhibits the intracellular burst of reactive oxygen species (ROS) that occurs after reoxygenation of vascular smooth muscle cells. Reactive Oxygen Species 141-164 Rac family small GTPase 1 Homo sapiens 77-81 9576744-1 1998 We demonstrate that adenoviral-mediated gene transfer of a dominant negative rac1 gene product (N17rac1) inhibits the intracellular burst of reactive oxygen species (ROS) that occurs after reoxygenation of vascular smooth muscle cells. Reactive Oxygen Species 166-169 Rac family small GTPase 1 Homo sapiens 77-81 8670049-1 1996 On neutrophil stimulation, the cytosolic components of NADPH oxidase, p67phox, p47phox, p40phox, as well as the Ras-related G-proteins Rac1 and Rac2, are translocated from the cytosol to cell membranes where they associate with a flavocytochrome b, forming a functional complex responsible for the production of oxygen radicals in phagocytes. Reactive Oxygen Species 312-327 Rac family small GTPase 1 Homo sapiens 135-139