PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32617075-8 2020 Passaged THP-1 cells, inheriting initial LPS challenge, presented with dysregulation of cytokine expression and oxygen consumption for up to 7 days after the initial LPS treatment. Oxygen 112-118 GLI family zinc finger 2 Homo sapiens 9-14 15585204-8 2005 Furthermore hypoxia (< or =1% O2) as a further proinflammatory and especially proangiogenetic factor was able to stimulate MIF secretion by THP-1, human monocytes and HUVECs. Oxygen 33-35 GLI family zinc finger 2 Homo sapiens 143-148 33244727-0 2021 Correction to: The inflammation and reactive oxygen species regulated by Nrf2 and NF-kappaB signaling pathways in 630-nm light-emitting diode irradiation treated THP-1 monocytes/macrophages. Oxygen 45-51 GLI family zinc finger 2 Homo sapiens 162-167 33128166-0 2021 The inflammation and reactive oxygen species regulated by Nrf2 and NF-kappaB signaling pathways in 630-nm light-emitting diode irradiation treated THP-1 monocytes/macrophages. Oxygen 30-36 GLI family zinc finger 2 Homo sapiens 147-152 32655788-7 2020 In vitro IHR stimuli in human monocytic THP-1 cells resulted in gene promoter hypomethylation-mediated FPR1 over-expression, increased production of reactive oxygen species, and increased cell apoptosis, which could be reversed with re-methylation agent, folic acid, treatment. Oxygen 158-164 GLI family zinc finger 2 Homo sapiens 40-45 10223943-9 1999 We conclude that (i) the control exerted by gamma interferon on intracellular multiplication of Listeria in THP-1 macrophages is dependent on the production of nitric oxide and hydrogen peroxide; (ii) intracellular Listeria may become insensitive to ampicillin in macrophages exposed to gamma interferon because the increase in reactive oxygen and nitrogen intermediates already controls bacterial growth; and (iii) azithromycin and still more sparfloxacin cooperate efficiently with gamma interferon, one of the main cellular host defenses in Listeria infection. Oxygen 337-343 GLI family zinc finger 2 Homo sapiens 108-113 10419182-0 1999 Vitamin E inhibition of O2*- production in the promonocyte cell line THP-1 is essentially due to RRR-delta-tocopherol. Oxygen 24-26 GLI family zinc finger 2 Homo sapiens 69-74 31707353-8 2020 Impaired inflammasome activation in G6PD-kd THP-1 cells was mediated by a decrease in the production of reactive oxygen species (ROS) by NOX signaling, while treatment with hydrogen peroxide (H2O2) enhanced inflammasome activation in G6PD-kd THP-1 cells. Oxygen 113-119 GLI family zinc finger 2 Homo sapiens 44-49 28120861-4 2017 By comparing the molecular responses of macrophages derived from THP1 monocytes to both types of CNTs, we highlight a molecular mechanism regulated by Nrf2/Bach1 signaling pathways to induce CNT degradation via NOX2 complex activation and O2 -, H2O2 and OH production. Oxygen 239-241 GLI family zinc finger 2 Homo sapiens 65-69 28584285-3 2017 A helium/oxygen radio frequency driven atmospheric plasma profoundly induced apoptosis in THP-1 cells whereas helium, humidified helium, and humidified helium/oxygen plasmas were inefficient. Oxygen 9-15 GLI family zinc finger 2 Homo sapiens 90-95 28584285-0 2017 Oxygen atoms are critical in rendering THP-1 leukaemia cells susceptible to cold physical plasma-induced apoptosis. Oxygen 0-6 GLI family zinc finger 2 Homo sapiens 39-44 23355903-0 2013 Oxygen tension modulates differentiation and primary macrophage functions in the human monocytic THP-1 cell line. Oxygen 0-6 GLI family zinc finger 2 Homo sapiens 97-102 23355903-5 2013 However, decreasing the oxygen tension to 5% O2 significantly increased the rate of phorbol ester-induced differentiation of THP-1 cells into macrophage-like cells as well as the metabolic activity of both undifferentiated and PMA-differentiated THP-1 cells. Oxygen 24-30 GLI family zinc finger 2 Homo sapiens 125-130 23355903-5 2013 However, decreasing the oxygen tension to 5% O2 significantly increased the rate of phorbol ester-induced differentiation of THP-1 cells into macrophage-like cells as well as the metabolic activity of both undifferentiated and PMA-differentiated THP-1 cells. Oxygen 24-30 GLI family zinc finger 2 Homo sapiens 246-251 23355903-5 2013 However, decreasing the oxygen tension to 5% O2 significantly increased the rate of phorbol ester-induced differentiation of THP-1 cells into macrophage-like cells as well as the metabolic activity of both undifferentiated and PMA-differentiated THP-1 cells. Oxygen 45-47 GLI family zinc finger 2 Homo sapiens 125-130 23355903-5 2013 However, decreasing the oxygen tension to 5% O2 significantly increased the rate of phorbol ester-induced differentiation of THP-1 cells into macrophage-like cells as well as the metabolic activity of both undifferentiated and PMA-differentiated THP-1 cells. Oxygen 45-47 GLI family zinc finger 2 Homo sapiens 246-251 23355903-7 2013 In differentiated THP-1 cells, lowering the oxygen tension to 5% O2 decreased phagocytic activity, the constitutive release of beta-hexosaminidase and LPS-induced NF-kappaB activation but enhanced LPS-stimulated release of cytokines. Oxygen 44-50 GLI family zinc finger 2 Homo sapiens 18-23 23355903-7 2013 In differentiated THP-1 cells, lowering the oxygen tension to 5% O2 decreased phagocytic activity, the constitutive release of beta-hexosaminidase and LPS-induced NF-kappaB activation but enhanced LPS-stimulated release of cytokines. Oxygen 65-67 GLI family zinc finger 2 Homo sapiens 18-23 23355903-8 2013 Collectively, these data demonstrate that oxygen tension influences THP-1 cell differentiation and primary macrophage functions, and suggest that culturing these cells under tightly regulated oxygen tension in the absence of exogenous reducing agent and serum is likely to provide a physiologically relevant baseline from which to study the role of the local redox environment in regulating THP-1 cell physiology. Oxygen 42-48 GLI family zinc finger 2 Homo sapiens 68-73