PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10679259-1 2000 The replacement of heme iron by cobalt or nickel in a putative oxygen sensor is supposed to reduce oxygen binding to the heme protein, resulting in HIF-1 activation and erythropoietin (EPO) induction. Nickel 42-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 148-153 10646848-2 2000 Here we have demonstrated that nickel exposure induced hypoxic signaling pathways by inducing hypoxia-inducible transcription factor-1 (HIF-1), which mediated the induction of genes required by cells to survive hypoxia. Nickel 31-37 hypoxia inducible factor 1 subunit alpha Homo sapiens 94-134 10646848-2 2000 Here we have demonstrated that nickel exposure induced hypoxic signaling pathways by inducing hypoxia-inducible transcription factor-1 (HIF-1), which mediated the induction of genes required by cells to survive hypoxia. Nickel 31-37 hypoxia inducible factor 1 subunit alpha Homo sapiens 136-141 10646848-3 2000 We also show that a new gene, Cap43, is dependent upon HIF-1 because only HIF-1-proficient cells induced Cap43 when exposed to either hypoxia or nickel. Nickel 145-151 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-60 10646848-3 2000 We also show that a new gene, Cap43, is dependent upon HIF-1 because only HIF-1-proficient cells induced Cap43 when exposed to either hypoxia or nickel. Nickel 145-151 hypoxia inducible factor 1 subunit alpha Homo sapiens 74-79 10646848-4 2000 We also show that glyceraldehyde-3-phosphate dehydrogenase, a gene induced by hypoxia through HIF-1, was similar to Cap43 in that it required HIF-1-proficient cells to be induced by either nickel or hypoxia. Nickel 189-195 hypoxia inducible factor 1 subunit alpha Homo sapiens 94-99 10646848-4 2000 We also show that glyceraldehyde-3-phosphate dehydrogenase, a gene induced by hypoxia through HIF-1, was similar to Cap43 in that it required HIF-1-proficient cells to be induced by either nickel or hypoxia. Nickel 189-195 hypoxia inducible factor 1 subunit alpha Homo sapiens 142-147 10469629-0 1999 Nickel-induced transformation shifts the balance between HIF-1 and p53 transcription factors. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 57-62 34571076-12 2021 We also showed that nickel-induced TET1 was stimulated by HIF-1alpha. Nickel 20-26 hypoxia inducible factor 1 subunit alpha Homo sapiens 58-68 32566089-7 2020 N-Acetylcysteine (NAC) manifested similar effects as melatonin in scavenging ROS, maintaining prolyl-hydroxylase activity, and mitigating HIF-1alpha transcriptional activity in nickel-exposed cells. Nickel 177-183 hypoxia inducible factor 1 subunit alpha Homo sapiens 138-148 33740985-4 2021 In this study, we proposed that exposure of human epidermal keratinocytes (HaCaT) to metal nanoparticles, such as nickel nanoparticles, dysregulates tight-junction associated proteins by interacting with the HIF-1alpha/miR-29b/MMPs axis. Nickel 114-120 hypoxia inducible factor 1 subunit alpha Homo sapiens 208-218 32566089-0 2020 Melatonin Antagonizes Nickel-Induced Aerobic Glycolysis by Blocking ROS-Mediated HIF-1alpha/miR210/ISCU Axis Activation. Nickel 22-28 hypoxia inducible factor 1 subunit alpha Homo sapiens 81-91 32566089-1 2020 Nickel and its compounds, which are well-documented carcinogens, induce the Warburg effect in normal cells by stabilizing hypoxia-inducible factor 1alpha (HIF-1alpha). Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 122-153 32566089-1 2020 Nickel and its compounds, which are well-documented carcinogens, induce the Warburg effect in normal cells by stabilizing hypoxia-inducible factor 1alpha (HIF-1alpha). Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 155-165 32566089-8 2020 Our results indicated that ROS generation contributed to nickel-caused HIF-1alpha stabilization and downstream signal activation. Nickel 57-63 hypoxia inducible factor 1 subunit alpha Homo sapiens 71-81 28263966-4 2017 Our present study, for the first time to the best of our knowledge, discovered that environmental carcinogen nickel exposure led to MEG3 downregulation, consequently initiating c-Jun-mediated PHLPP1 transcriptional inhibition and hypoxia-inducible factor-1alpha (HIF-1alpha) protein translation upregulation, in turn resulting in malignant transformation of human bronchial epithelial cells. Nickel 109-115 hypoxia inducible factor 1 subunit alpha Homo sapiens 230-261 31804169-3 2020 DISCUSSION: Nickel and oxidative stress: Nickel alters intracellular chemical microenvironment by increasing ionized calcium concentration, lipid peroxidation, cyclooxygenase, constitutive nitric oxide synthase, leukotriene B4, prostaglandin E2, interleukins, tumor necrosis factor-alpha, caspases, complement activation, heat shock protein 70 kDa and hypoxia-inducible factor-1alpha. Nickel 41-47 hypoxia inducible factor 1 subunit alpha Homo sapiens 322-383 29355601-0 2018 Nickel ions bind to HSP90beta and enhance HIF-1alpha-mediated IL-8 expression. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 42-52 31963541-0 2020 Metformin Mitigates Nickel-Elicited Angiopoietin-Like Protein 4 Expression via HIF-1alpha for Lung Tumorigenesis. Nickel 20-26 hypoxia inducible factor 1 subunit alpha Homo sapiens 79-89 31963541-8 2020 In conclusion, the increased presence of ANGPTL4 due to HIF-1alpha accumulation that is caused by nickel in lung cells may be one mechanism by which nickel exposure contributes to lung cancer progression. Nickel 98-104 hypoxia inducible factor 1 subunit alpha Homo sapiens 56-66 31963541-8 2020 In conclusion, the increased presence of ANGPTL4 due to HIF-1alpha accumulation that is caused by nickel in lung cells may be one mechanism by which nickel exposure contributes to lung cancer progression. Nickel 149-155 hypoxia inducible factor 1 subunit alpha Homo sapiens 56-66 28552779-1 2017 Nickel is a human carcinogen that acts as a hypoxia mimic by activating the transcription factor HIF-1alpha and hypoxia-like transcriptomic responses. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 97-107 28263966-4 2017 Our present study, for the first time to the best of our knowledge, discovered that environmental carcinogen nickel exposure led to MEG3 downregulation, consequently initiating c-Jun-mediated PHLPP1 transcriptional inhibition and hypoxia-inducible factor-1alpha (HIF-1alpha) protein translation upregulation, in turn resulting in malignant transformation of human bronchial epithelial cells. Nickel 109-115 hypoxia inducible factor 1 subunit alpha Homo sapiens 263-273 28263966-6 2017 Moreover, HIF-1alpha protein translation was upregulated via activating the Akt/p70S6K/S6 axis resultant from PHLPP1 inhibition in nickel responses. Nickel 131-137 hypoxia inducible factor 1 subunit alpha Homo sapiens 10-20 28263966-7 2017 Collectively, we uncover that nickel exposure results in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun and in turn increasing c-Jun inhibition of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1alpha protein translation, as well as malignant transformation of human bronchial epithelial cells. Nickel 30-36 hypoxia inducible factor 1 subunit alpha Homo sapiens 288-298 28004401-8 2017 Agents such as iron chelators, and heavy metals like cobalt and nickel were demonstrated to be effective in maintaining the HIF-1alpha level in the nerve. Nickel 64-70 hypoxia inducible factor 1 subunit alpha Homo sapiens 124-134 25614230-5 2015 Furthermore, nickel exposure increased the expression of hypoxia-inducible-factor-1alpha (HIF-1alpha) and induced the activation of the AKT/PKB kinase pathway, as shown by the increase of P(Ser-9)-GSK-3beta, the inactive form of glycogen synthase kinase-3beta (GSK-3beta). Nickel 13-19 hypoxia inducible factor 1 subunit alpha Homo sapiens 57-88 26051273-6 2015 Nickel is a known hypoxia-mimetic that activates hypoxia inducible factor-1alpha (HIF1alpha). Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 49-80 26051273-6 2015 Nickel is a known hypoxia-mimetic that activates hypoxia inducible factor-1alpha (HIF1alpha). Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 82-91 26051273-7 2015 Nickel-induced inhibition of fatty acid oxidation was blunted in HIF1alpha knockout fibroblasts, implicating HIF1alpha as one contributor to the mechanism. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 65-74 26051273-7 2015 Nickel-induced inhibition of fatty acid oxidation was blunted in HIF1alpha knockout fibroblasts, implicating HIF1alpha as one contributor to the mechanism. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 109-118 25614230-5 2015 Furthermore, nickel exposure increased the expression of hypoxia-inducible-factor-1alpha (HIF-1alpha) and induced the activation of the AKT/PKB kinase pathway, as shown by the increase of P(Ser-9)-GSK-3beta, the inactive form of glycogen synthase kinase-3beta (GSK-3beta). Nickel 13-19 hypoxia inducible factor 1 subunit alpha Homo sapiens 90-100 23828170-10 2013 We found that HSP90AA1, one of the main modulators, interacted with HIF1A, AR and BCL2 in nickel-exposed cells. Nickel 90-96 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-73 24497960-5 2014 Cobalt and nickel induced a concentration-dependent increase of OCT4 and HIF-1alpha, but not NANOG or KLF4. Nickel 11-17 hypoxia inducible factor 1 subunit alpha Homo sapiens 73-83 22133446-0 2011 Nickel ENMs activate HIF-1alpha. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 21-31 23526216-0 2013 Role of hypoxia-inducible factor 1, alpha subunit and cAMP-response element binding protein 1 in synergistic release of interleukin 8 by prostaglandin E2 and nickel in lung fibroblasts. Nickel 158-164 hypoxia inducible factor 1 subunit alpha Homo sapiens 8-49 22910906-3 2012 In this study, it was found that a deficiency of JNK2 expression reduced HIF-1alpha protein induction in response to nickel treatment resulting from the impaired expression of hif-1alpha mRNA. Nickel 117-123 hypoxia inducible factor 1 subunit alpha Homo sapiens 73-83 22910906-3 2012 In this study, it was found that a deficiency of JNK2 expression reduced HIF-1alpha protein induction in response to nickel treatment resulting from the impaired expression of hif-1alpha mRNA. Nickel 117-123 hypoxia inducible factor 1 subunit alpha Homo sapiens 176-186 32260803-1 2013 Nickel and cobalt are both known to stimulate the hypoxia-inducible factor-1 (HIF-1alpha), thus significantly improving blood vessel formation in tissue engineering applications. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 78-88 21401309-0 2011 The role of hypoxia inducible factor-1alpha in the increased MMP-2 and MMP-9 production by human monocytes exposed to nickel nanoparticles. Nickel 118-124 hypoxia inducible factor 1 subunit alpha Homo sapiens 12-43 21828359-6 2011 In contrast to no response to metallic Ni microparticles, nickel nanoparticles caused a rapid and prolonged activation of the HIF-1alpha pathway that was stronger than that induced by soluble Ni(II). Nickel 58-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 126-136 20046830-6 2009 Interestingly, knockdown of both HIF-1alpha and HIF-2alpha attenuated c-Myc degradation induced by Nickel and hypoxia, suggesting the functional HIF-1alpha and HIF-2alpha was required for c-myc degradation. Nickel 99-105 hypoxia inducible factor 1 subunit alpha Homo sapiens 33-43 20046830-6 2009 Interestingly, knockdown of both HIF-1alpha and HIF-2alpha attenuated c-Myc degradation induced by Nickel and hypoxia, suggesting the functional HIF-1alpha and HIF-2alpha was required for c-myc degradation. Nickel 99-105 hypoxia inducible factor 1 subunit alpha Homo sapiens 145-155 16649251-2 2006 One major consequence of exposure to nickel is the stabilization of hypoxia inducible factor-1alpha (HIF-1alpha), a protein known to be overexpressed in a variety of cancers. Nickel 37-43 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-99 17382205-0 2007 The role of ascorbate in the modulation of HIF-1alpha protein and HIF-dependent transcription by chromium(VI) and nickel(II). Nickel 114-120 hypoxia inducible factor 1 subunit alpha Homo sapiens 43-53 17382205-9 2007 These data correlate with extended stabilization of HIF-1alpha after acute exposure to nickel(II). Nickel 87-93 hypoxia inducible factor 1 subunit alpha Homo sapiens 52-62 16877034-8 2006 If treatment with the Fe and metal ions was simultaneous (co-treatment), the effects of nickel ion exposure were overwhelmed, since the added Fe reversed HIF-1alpha stabilization, decreased IRP-1 activity, and increased ferritin level. Nickel 88-94 hypoxia inducible factor 1 subunit alpha Homo sapiens 154-164 19505905-5 2009 In addition, we verified that hypoxia-inducible factor-1alpha, an important transcription factor of nickel response, was not required for the cyclin D1 or cyclin E induction. Nickel 100-106 hypoxia inducible factor 1 subunit alpha Homo sapiens 30-61 18832182-0 2009 Nickel and the microbial toxin, MALP-2, stimulate proangiogenic mediators from human lung fibroblasts via a HIF-1alpha and COX-2-mediated pathway. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 108-118 17312168-4 2007 The bulk of those genes were identified as targets of two distinct signaling cascades, the IKK2/NF-kappaB pathway and a proangiogenic pathway mediated by HIF-1alpha, which accumulates upon exposure to nickel. Nickel 201-207 hypoxia inducible factor 1 subunit alpha Homo sapiens 154-164 17312168-7 2007 Nickel-dependent HIF-1alpha activation primarily modulates expression of genes involved in proliferation, survival, metabolism, and signaling, albeit the induction of some proinflammatory nickel-response genes, most prominently IL-6, which we identified as novel bona fide HIF-1alpha target in this study, is also critically dependent on this pathway. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 17-27 17312168-7 2007 Nickel-dependent HIF-1alpha activation primarily modulates expression of genes involved in proliferation, survival, metabolism, and signaling, albeit the induction of some proinflammatory nickel-response genes, most prominently IL-6, which we identified as novel bona fide HIF-1alpha target in this study, is also critically dependent on this pathway. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 273-283 17312168-9 2007 Taken together, our data provide mechanistic insight into the complex network of nickel-induced cellular events and identify IKK2/NF-kappaB and HIF-1alpha as important pathways involved in processes such as delivery of "second signals" in contact hypersensitivity reactions to nickel. Nickel 81-87 hypoxia inducible factor 1 subunit alpha Homo sapiens 144-154 16288478-5 2006 Nickel exposure caused strong activation of HIF-1alpha and HIF-2alpha proteins, underscoring activation of HIF-1-dependent transcription. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 44-49 16649251-2 2006 One major consequence of exposure to nickel is the stabilization of hypoxia inducible factor-1alpha (HIF-1alpha), a protein known to be overexpressed in a variety of cancers. Nickel 37-43 hypoxia inducible factor 1 subunit alpha Homo sapiens 101-111 16649251-3 2006 In this study, we report a persistent stabilization of HIF-1alpha by nickel chloride up to 72 h after the removal of nickel from the culture media. Nickel 69-75 hypoxia inducible factor 1 subunit alpha Homo sapiens 55-65 16649251-8 2006 Understanding the mechanisms by which nickel can inhibit HIF-PHD"s and stabilize HIF-1alpha may be important in the treatment of cancer and ischemic diseases. Nickel 38-44 hypoxia inducible factor 1 subunit alpha Homo sapiens 81-91 15866766-8 2005 Nickel depletes intracellular ascorbate, which leads to the inhibition of cellular hydroxylases, manifested by the loss of hypoxia-inducible factor (HIF)-1alpha and -2alpha hydroxylation and hypoxia-like stress. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 123-172 16283525-4 2005 Nickel may interfere with iron at both an extracellular level, by preventing iron from being transported into the cell, and at an intracellular level, by competing for iron sites on enzymes like the prolyl hydroxylases that modify hypoxia inducible factor-1alpha (HIF-1alpha). Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 231-262 16283525-4 2005 Nickel may interfere with iron at both an extracellular level, by preventing iron from being transported into the cell, and at an intracellular level, by competing for iron sites on enzymes like the prolyl hydroxylases that modify hypoxia inducible factor-1alpha (HIF-1alpha). Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 264-274 16283525-5 2005 Nickel was able to decrease the binding of the Von Hippel-Lindau (VHL) protein to HIF-1alpha, indicating a decrease in prolyl hydroxylase activity. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 82-92 16283525-7 2005 In addition, understanding the mechanisms by which nickel activates the HIF-1alpha pathway may lead to new molecular targets in fighting cancer. Nickel 51-57 hypoxia inducible factor 1 subunit alpha Homo sapiens 72-82 16039939-1 2005 Nickel (Ni) compounds are well-established carcinogens and are known to initiate a hypoxic response in cells via the stabilization and transactivation of hypoxia-inducible factor-1 alpha (HIF-1alpha). Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 154-186 16039939-1 2005 Nickel (Ni) compounds are well-established carcinogens and are known to initiate a hypoxic response in cells via the stabilization and transactivation of hypoxia-inducible factor-1 alpha (HIF-1alpha). Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 188-198 14726713-6 2004 Iron is central to the oxygen sensing mechanism, and sensitivity to other metals, namely cobalt and nickel, is a distinctive feature of the HIF system; in fact, this is often used as an initial way of implicating HIF-1 in a biological response. Nickel 100-106 hypoxia inducible factor 1 subunit alpha Homo sapiens 213-218 16705796-1 2005 Although nickel and cobalt compounds have been known to cause induction of the transcription factor hypoxia-inducible factor 1 (HIF-1) and activation of a battery of hypoxia-inducible genes in the cell, the molecular mechanisms of this induction remain unclear. Nickel 9-15 hypoxia inducible factor 1 subunit alpha Homo sapiens 100-126 16705796-1 2005 Although nickel and cobalt compounds have been known to cause induction of the transcription factor hypoxia-inducible factor 1 (HIF-1) and activation of a battery of hypoxia-inducible genes in the cell, the molecular mechanisms of this induction remain unclear. Nickel 9-15 hypoxia inducible factor 1 subunit alpha Homo sapiens 128-133 14729612-5 2004 Inhibition of PI-3K, Akt, and p70(S6k) by overexpression of a dominant-negative mutant of PI-3K (Deltap85) impaired nickel-induced HIF-1 transactivation. Nickel 116-122 hypoxia inducible factor 1 subunit alpha Homo sapiens 131-136 14729612-6 2004 Furthermore, an overexpression of the dominant-negative Akt mutant (Akt-T308A/S473A) blocked nickel-induced Akt phosphorylation and HIF-1 transactivation, whereas inhibition of p70(S6k) activation by pretreatment of cells with rapamycin did not show significant inhibitory effects on HIF-1 transactivation induced by nickel compounds. Nickel 93-99 hypoxia inducible factor 1 subunit alpha Homo sapiens 132-137 14729612-6 2004 Furthermore, an overexpression of the dominant-negative Akt mutant (Akt-T308A/S473A) blocked nickel-induced Akt phosphorylation and HIF-1 transactivation, whereas inhibition of p70(S6k) activation by pretreatment of cells with rapamycin did not show significant inhibitory effects on HIF-1 transactivation induced by nickel compounds. Nickel 93-99 hypoxia inducible factor 1 subunit alpha Homo sapiens 284-289 14729612-8 2004 These results demonstrated that nickel compounds induce HIF-1 transactivation and Cap43 protein expression through a PI-3K/Akt-dependent and p70(S6k)-independent pathway. Nickel 32-38 hypoxia inducible factor 1 subunit alpha Homo sapiens 56-61 12839937-5 2003 Acute exposure to nickel resulted in the accumulation of hypoxia-inducible transcription factor (HIF)-1, which strongly activated hypoxia-inducible genes, including the recently discovered tumor marker NDRG1 (Cap43). Nickel 18-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 57-103 14645679-0 2003 Hypoxia inducible factor-1 alpha-independent suppression of aryl hydrocarbon receptor-regulated genes by nickel. Nickel 105-111 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-32 12839937-6 2003 To further identify HIF-1-dependent nickel-inducible genes and to understand the role of the HIF-dependent signaling pathway in nickel-induced transformation, we used the Affymetrix GeneChip to compare the gene expression profiles in wild-type cells or in cells from HIF-1 alpha knockout mouse embryos exposed to nickel chloride. Nickel 36-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 20-25 12839937-7 2003 As expected, when we examined 12,000 genes for expression changes, we found that genes coding for glycolytic enzymes and glucose transporters, known to be regulated by HIF-1 transcription factor, were induced by nickel only in HIF-1 alpha-proficient cells. Nickel 212-218 hypoxia inducible factor 1 subunit alpha Homo sapiens 168-173 12839937-7 2003 As expected, when we examined 12,000 genes for expression changes, we found that genes coding for glycolytic enzymes and glucose transporters, known to be regulated by HIF-1 transcription factor, were induced by nickel only in HIF-1 alpha-proficient cells. Nickel 212-218 hypoxia inducible factor 1 subunit alpha Homo sapiens 227-238 12839937-9 2003 Additionally, we found a number of genes induced by nickel in a HIF-independent manner, suggesting that Ni activated other signaling pathways besides HIF-1. Nickel 52-58 hypoxia inducible factor 1 subunit alpha Homo sapiens 150-155 12839937-10 2003 Finally, we found that in HIF-1 alpha knockout cells, nickel strongly induced the expression of the whole group of genes that were not expressed in the presence of HIF-1. Nickel 54-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-37 12839937-10 2003 Finally, we found that in HIF-1 alpha knockout cells, nickel strongly induced the expression of the whole group of genes that were not expressed in the presence of HIF-1. Nickel 54-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-31 12839937-11 2003 Because the majority of modulated genes were induced or suppressed by nickel in a HIF-1-dependent manner, we elucidated the role of HIF-1 transcription factor in cell transformation. Nickel 70-76 hypoxia inducible factor 1 subunit alpha Homo sapiens 82-87 12839937-11 2003 Because the majority of modulated genes were induced or suppressed by nickel in a HIF-1-dependent manner, we elucidated the role of HIF-1 transcription factor in cell transformation. Nickel 70-76 hypoxia inducible factor 1 subunit alpha Homo sapiens 132-137 12839937-12 2003 In HIF-1 alpha-proficient cells, nickel exposure increased soft agar growth, whereas it decreased soft agar growth in HIF-1 alpha-deficient cells. Nickel 33-39 hypoxia inducible factor 1 subunit alpha Homo sapiens 3-14 12839937-13 2003 We hypothesize that the induction of HIF-1 transcription factor by nickel may be important during the nickel-induced carcinogenic process. Nickel 67-73 hypoxia inducible factor 1 subunit alpha Homo sapiens 37-42 12839937-13 2003 We hypothesize that the induction of HIF-1 transcription factor by nickel may be important during the nickel-induced carcinogenic process. Nickel 102-108 hypoxia inducible factor 1 subunit alpha Homo sapiens 37-42 11739637-3 2001 Other than hypoxia, cobalt and nickel, which can substitute for iron in the ferroprotein, induce the stabilization of HIF-1alpha and the activation of HIF-1. Nickel 31-37 hypoxia inducible factor 1 subunit alpha Homo sapiens 118-128 12729255-8 2003 For example, both nickel compounds activated a number of transcription factors including hypoxia-inducible factor I (HIF-1) and p53. Nickel 18-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 117-122 12729255-10 2003 The obtained data are in agreement with our previous observations that acute nickel exposure activates HIF-1 and p53 transcription factors and in nickel-transformed cells, the ratio of HIF-I activity to p53 activity was shifted towards high HIF-I activity. Nickel 77-83 hypoxia inducible factor 1 subunit alpha Homo sapiens 103-108 12426141-2 2002 Acute exposure to nickel activates hypoxia-inducible transcription factor-1 (HIF-1), which strongly induces hypoxia-inducible genes, including the recently discovered tumor marker Cap43. Nickel 18-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 35-75 12426141-2 2002 Acute exposure to nickel activates hypoxia-inducible transcription factor-1 (HIF-1), which strongly induces hypoxia-inducible genes, including the recently discovered tumor marker Cap43. Nickel 18-24 hypoxia inducible factor 1 subunit alpha Homo sapiens 77-82 12426141-4 2002 To identify other HIF-1-dependent/independent nickel-inducible genes, we used cells obtained from HIF-1 alpha null mouse embryos and analyzed gene expression changes using the microarray technique. Nickel 46-52 hypoxia inducible factor 1 subunit alpha Homo sapiens 18-23 12426141-5 2002 We found that genes coding for glycolytic enzymes, known to be regulated by HIF-1, were also induced in nickel-exposed cells. Nickel 104-110 hypoxia inducible factor 1 subunit alpha Homo sapiens 76-81 12426141-7 2002 Elevated HIF-1 activity after acute nickel exposure might be selectively advantageous because nickel-transformed rodent and human cells possess increased HIF-1 transcriptional activity. Nickel 36-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 9-14 12426141-7 2002 Elevated HIF-1 activity after acute nickel exposure might be selectively advantageous because nickel-transformed rodent and human cells possess increased HIF-1 transcriptional activity. Nickel 36-42 hypoxia inducible factor 1 subunit alpha Homo sapiens 154-159 12426141-7 2002 Elevated HIF-1 activity after acute nickel exposure might be selectively advantageous because nickel-transformed rodent and human cells possess increased HIF-1 transcriptional activity. Nickel 94-100 hypoxia inducible factor 1 subunit alpha Homo sapiens 9-14 12426141-7 2002 Elevated HIF-1 activity after acute nickel exposure might be selectively advantageous because nickel-transformed rodent and human cells possess increased HIF-1 transcriptional activity. Nickel 94-100 hypoxia inducible factor 1 subunit alpha Homo sapiens 154-159 11779168-1 2002 Treatment with divalent metal ions such as cobalt (Co(2+)) or nickel (Ni(2+)) result in the stabilization of hypoxia-inducible factor-1alpha (HIF1alpha). Nickel 62-68 hypoxia inducible factor 1 subunit alpha Homo sapiens 109-140 11779168-1 2002 Treatment with divalent metal ions such as cobalt (Co(2+)) or nickel (Ni(2+)) result in the stabilization of hypoxia-inducible factor-1alpha (HIF1alpha). Nickel 62-68 hypoxia inducible factor 1 subunit alpha Homo sapiens 142-151 11739637-3 2001 Other than hypoxia, cobalt and nickel, which can substitute for iron in the ferroprotein, induce the stabilization of HIF-1alpha and the activation of HIF-1. Nickel 31-37 hypoxia inducible factor 1 subunit alpha Homo sapiens 118-123 11504687-0 2001 Nickel requires hypoxia-inducible factor-1 alpha, not redox signaling, to induce plasminogen activator inhibitor-1. Nickel 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 16-48 11504687-4 2001 The involvement of the NADPH oxidase complex, reactive oxygen species, and kinases in mediating nickel-induced HIF-1 alpha signaling was also investigated. Nickel 96-102 hypoxia inducible factor 1 subunit alpha Homo sapiens 111-122 11504687-5 2001 Addition of nickel to BEAS-2B human airway epithelial cells increased HIF-1 alpha protein levels and elevated PAI-1 mRNA levels. Nickel 12-18 hypoxia inducible factor 1 subunit alpha Homo sapiens 70-81 11504687-6 2001 Pretreatment of cells with the extracellular signal-regulated kinase inhibitor U-0126 partially blocked HIF-1 alpha protein and PAI-1 mRNA levels induced by nickel, whereas antioxidants and NADPH oxidase inhibitors had no effect. Nickel 157-163 hypoxia inducible factor 1 subunit alpha Homo sapiens 104-115 11504687-7 2001 Pretreating cells with antisense, but not sense, oligonucleotides to HIF-1 alpha mRNA abolished nickel-stimulated increases in PAI-1 mRNA. Nickel 96-102 hypoxia inducible factor 1 subunit alpha Homo sapiens 69-80 11504687-8 2001 These data indicate that signaling through extracellular signal-regulated kinase and HIF-1 alpha is required for nickel-induced transcriptional activation of PAI-1. Nickel 113-119 hypoxia inducible factor 1 subunit alpha Homo sapiens 85-96