| Name | c jun |
|---|---|
| Synonyms | AP1; Activator protein 1; JUN; Proto oncogene c jun; Protooncogene c jun; Transcription factor AP 1; V jun avian sarcoma virus 17 oncogene homolog; c Jun… |
| Name | sodium arsenite |
|---|---|
| CAS | sodium arsenenite |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17938202 | Fung H, Liu P, Demple B: ATF4-dependent oxidative induction of the DNA repair enzyme Ape1 counteracts arsenite cytotoxicity and suppresses arsenite-mediated mutagenesis. Mol Cell Biol. 2007 Dec;27(24):8834-47. Epub 2007 Oct 15. We investigated expression of the essential base excision DNA repair enzyme apurinic endonuclease 1 (Ape1) in response to sodium arsenite. Electrophoretic mobility shift assays indicated that an ATF4/c-Jun heterodimer was the responsible transcription factor. |
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| 11353140 | Liu J, Kadiiska MB, Liu Y, Lu T, Qu W, Waalkes MP: Stress-related gene expression in mice treated with inorganic arsenicals. Toxicol Sci. 2001 Jun;61(2):314-20. Multiprobe RNase protection assay revealed the activation of the c-Jun/AP-1 transcription complex after arsenic treatments. Mice were injected sc with either sodium arsenite [As (III), 100 micromol/kg], arsenate [As (V), 300 micromol/kg], or saline. |
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| 10464319 | Iordanov MS, Magun BE: Different mechanisms of c-Jun NH (2)-terminal kinase-1 (JNK1) activation by ultraviolet-B radiation and by oxidative stressors. J Biol Chem. 1999 Sep 3;274(36):25801-6. The pro-oxidants sodium arsenite, cadmium and peroxide activated JNK1 with slow kinetics, whereas UV-B potentiated the activity of JNK1 rapidly. |
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| 14962100 | Liao WT, Chang KL, Yu CL, Chen GS, Chang LW, Yu HS: Arsenic induces human keratinocyte apoptosis by the FAS/FAS ligand pathway, which correlates with alterations in nuclear factor-kappa B and activator protein-1 activity. J Invest Dermatol. 2004 Jan;122(1):125-9. To investigate the mechanism of arsenic-induced apoptosis and related alterations in NF-kappa B and AP-1 activity, we exposed cultured human foreskin keratinocytes to different concentrations of sodium arsenite. |
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| 15849723 | Felix K, Manna SK, Wise K, Barr J, Ramesh GT: Low levels of arsenite activates nuclear factor-kappaB and activator protein-1 in immortalized mesencephalic cells. J Biochem Mol Toxicol. 2005 Mar-Apr;19(2):67-77. These mesencephalic cells were treated with low concentrations of sodium arsenite (0.1, 0.5, 1, 5, and 10 microM) and incubated for different periods of time (0-4 h). |
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| 9837857 | Hartsfield CL, Alam J, Choi AM: Transcriptional regulation of the heme oxygenase 1 gene by pyrrolidine dithiocarbamate. FASEB J. 1998 Dec;12(15):1675-82. Heme oxygenase 1 (HO-1), a stress response protein, is highly induced in response to various agents causing oxidative stress including ultraviolet irradiation, sodium arsenite, hyperoxia, and depletors. Mutational analyses of this enhancer showed that the activator protein 1 (AP-1) regulatory element is crucial for PDTC-induced HO-1 gene transcription. |
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| 12210719 | Li M, Cai JF, Chiu JF: Arsenic induces oxidative stress and activates stress gene expressions in cultured lung epithelial cells. J Cell Biochem. 2002;87(1):29-38. Significant elevations in c-fos and c-jun mRNA levels were observed within 30 min after exposure to arsenic and by enhancement of AP-1 DNA binding activity and transactivation activity. |
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| 12639917 | Vandeput F, Perpete S, Coulonval K, Lamy F, Dumont JE: Role of the different mitogen-activated protein kinase subfamilies in the stimulation of dog and human thyroid epithelial cell proliferation by cyclic 5'-monophosphate and growth factors. Endocrinology. 2003 Apr;144(4):1341-9. ERKs, c-Jun N-terminal kinases (JNKs), and p38 MAPK in the proliferation of dog and human thyroid epithelial cells (thyrocytes) in primary cultures. |
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| 16818494 | Cai B, Chang SH, Becker EB, Bonni A, Xia Z: p38 MAP kinase mediates apoptosis through phosphorylation of BimEL at Ser-65. J Biol Chem. 2006 Sep 1;281(35):25215-22. Epub 2006 Jul 3. The stress-activated c-Jun N-terminal protein kinase (JNK) and p38 mitogen-activated protein (MAP) kinase (p38) regulate apoptosis induced by several forms of cellular insults. Here we report evidence that sodium arsenite-induced apoptosis in PC12 cells may be due to direct phosphorylation of Bim (EL) at Ser-65 by p38. |
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| 10910055 | Simeonova PP, Wang S, Toriuma W, Kommineni V, Matheson J, Unimye N, Kayama F, Harki D, Ding M, Vallyathan V, Luster MI: Arsenic mediates cell proliferation and gene expression in the bladder epithelium: association with activating protein-1 transactivation. Cancer Res. 2000 Jul 1;60(13):3445-53. In the current studies, we demonstrate that mice exposed to 0.01% sodium arsenite in drinking water develop hyperplasia of the bladder urothelium within 4 weeks of exposure. Gene expression studies using RNase protection assays, reverse transcription-PCR, and cDNA microarrays indicated that arsenite alters the expression of a number of genes associated with cell growth, such as c-fos, c-jun, and EGR-1, as well as cell arrest, such as GADD153 and GADD45. |
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| 18629308 | Endo H, Sugioka Y, Nakagi Y, Saijo Y, Yoshida T: A novel role of the NRF2 transcription factor in the regulation of arsenite-mediated keratin 16 gene expression in human keratinocytes. Environ Health Perspect. 2008 Jul;116(7):873-9. BACKGROUND: Inorganic sodium arsenite (iAs) is a ubiquitous environmental contaminant and is associated with an increased risk of skin hyperkeratosis and cancer. We also found that the expression of K16 was transcriptionally induced by iAs through activator protein-1-like sites and an antioxidant response element (ARE) in its gene promoter region. |
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| 20071421 | Shinkai Y, Yamamoto C, Kaji T: Lead induces the expression of endoplasmic reticulum chaperones GRP78 and GRP94 in vascular endothelial cells via the JNK-AP-1 pathway. Toxicol Sci. 2010 Apr;114(2):378-86. Epub 2010 Jan 13. Interestingly, the lead-induced upregulation of GRP78 and GRP94 was almost completely blocked by the JNK inhibitor SP600125 or activator protein-1 (AP-1) inhibitor Compared with other metal (loid) s, including cadmium zinc and sodium arsenite, lead was found to be the most potent metal to induce these chaperones in endothelial cells. |
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| 17005224 | Hwang BJ, Utti C, Steinberg M: Induction of cyclin D1 by submicromolar concentrations of arsenite in human epidermal keratinocytes. Toxicol Appl Pharmacol. 2006 Dec 1;217(2):161-7. Epub 2006 Aug 11. To gain insight into the oncogenic properties of arsenic, we studied the expression of cyclin D1 in cultured human epidermal keratinocytes treated with submicromolar concentrations of sodium arsenite. Electrophoretic mobility shift assays (EMSA) showed that arsenite also stimulated binding of the transcription factors, AP1 and CREBP to their respective binding motifs within 3 days. |
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| 18404528 | Harada H, Sugimoto R, Watanabe A, Taketani S, Okada K, Warabi E, Siow R, Itoh K, Yamamoto M, Ishii T: Differential roles for Nrf2 and AP-1 in upregulation of HO-1 expression by arsenite in murine embryonic fibroblasts. Free Radic Res. 2008 Apr;42(4):297-304. Heme oxygenase-1 (HO-1) is markedly upregulated by sodium arsenite and previous studies implicated the transcriptional enhancers Nrf2 and AP-1 in arsenite-induced ho-1 gene expression in murine cells. The kinase inhibitor and JNK inhibitor SP600125 significantly attenuated arsenite induced increases in ho-1 mRNA levels in Nrf2 deficient cells but had negligible effects on Nrf2 activation, suggesting kinase/JNK/c-Jun plays a key role in the HO-1 upregulation via AP-1. |
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| 16451733 | Ryabinina OP, Subbian E, Iordanov MS: D-MEKK1, the Drosophila orthologue of mammalian MEKK4/MTK1, and Hemipterous/D-MKK7 mediate the activation of D-JNK by cadmium and arsenite in Schneider cells. BMC Cell Biol. 2006 Feb 1;7:7. BACKGROUND: The family of c-Jun NH2-terminal kinases (JNK) plays important roles in embryonic development and in cellular responses to stress. The mechanism of mammalian JNK activation by cadmium and sodium arsenite involves toxicant-induced oxidative stress. |
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| 17432879 | Hartsock WJ, Cohen JD, Segal DJ: Uranyl as a direct inhibitor of DNA-binding proteins. Chem Res Toxicol. 2007 May;20(5):784-9. Epub 2007 Apr 14. Inhibition of binding was apparent at 10 microM uranyl while no inhibition was observed with up to 2000 microM the cytotoxic metalloid sodium arsenite. Surprisingly, uranyl inhibited two nonzinc finger DNA-binding proteins, AP1 and NF-kappaB, to a similar extent, and zinc finger inhibition was reduced in the presence of bovine serum albumin. |
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| 16797887 | Suzuki T, Tsukamoto I: Arsenite induces apoptosis in hepatocytes through an enhancement of the activation of Jun N-terminal kinase and p38 mitogen-activated protein kinase caused by partial hepatectomy. Toxicol Lett. 2006 Sep 10;165(3):257-64. Epub 2006 May 12. To investigate the effects of arsenite on cell proliferation and the signal transduction in hapatocytes in vivo, rats received a single injection of sodium arsenite immediately after partial hepatectomy. The arsenite-injection markedly increased the phosphorylated forms of c-Jun and ATF-2 and the protein levels of c-Jun, p53 and p21 (WAF1/CIP1) in the partially hepatectomized liver. |
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| 11807011 | Werz O, Burkert E, Samuelsson B, Radmark O, Steinhilber D: Activation of 5-lipoxygenase by cell stress is independent in human polymorphonuclear leukocytes. Blood. 2002 Feb 1;99(3):1044-52. This study showed that various forms of cell stress, such as chemical stress (sodium arsenite), osmotic stress, or heat shock lead to substantial formation of 5-LO products in freshly isolated human polymorphonuclear leukocytes (PMNLs), when exogenous (10 microM) was present. Only minor activation of extracellular signal-regulated kinases and c-jun NH (2)-terminal kinases was observed, implying that these MAPKs are less important for 5-LO product formation in stress-stimulated PMNLs. |
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| 11353137 | Wijeweera JB, Gandolfi AJ, Parrish A, Lantz RC: Sodium arsenite enhances AP-1 and NFkappaB DNA binding and induces stress protein expression in precision-cut rat lung slices. Toxicol Sci. 2001 Jun;61(2):283-94. |
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| 15741166 | Miralem T, Hu Z, Torno MD, Lelli KM, Maines MD: Small interference RNA-mediated gene silencing of human reductase, but not that of heme oxygenase-1, attenuates arsenite-mediated induction of the oxygenase and increases apoptosis in 293A kidney cells. J Biol Chem. 2005 Apr 29;280(17):17084-92. Epub 2005 Feb 28. Presently, small interference (si) RNA constructs were used to investigate the role of human BVR in sodium arsenite (As)-mediated induction of HO-1 and in cytoprotection against apoptosis. |
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| 12482858 | Duyndam MC, Hulscher ST, van der Wall E, Pinedo HM, Boven E: Evidence for a role of p38 kinase in hypoxia-inducible factor 1-independent induction of vascular endothelial growth factor expression by sodium arsenite. J Biol Chem. 2003 Feb 28;278(9):6885-95. Epub 2002 Dec 13. |
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| 10986282 | Yu R, Chen C, Mo YY, Hebbar V, Owuor ED, Tan TH, Kong AN: Activation of mitogen-activated protein kinase pathways induces antioxidant response element-mediated gene expression via a Nrf2-dependent mechanism. J Biol Chem. 2000 Dec 22;275(51):39907-13. Here, we report that the expression of mitogen-activated protein (MAP) kinase/extracellular signal-regulated kinase kinase kinase 1 (MEKK1), transforming growth factor-beta-activated kinase (TAK1), and apoptosis signal-regulating kinase (ASK1) in HepG2 cells activated the ARE reporter gene, whereas the expression of their dominant-negative mutants impaired ARE activation by the chemicals sodium arsenite and mercury |
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| 17961518 | DeFuria J, Shea TB: Arsenic inhibits neurofilament transport and induces perikaryal accumulation of phosphorylated neurofilaments: roles of JNK and GSK-3beta. Brain Res. 2007 Nov 21;1181:74-82. Epub 2007 Apr 12. We examined herein the impact of sodium arsenite (the inorganic form of arsenic) on NF dynamics. |
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| 11035063 | Hossain K, Akhand AA, Kato M, Du J, Takeda K, Wu J, Takeuchi K, Liu W, Suzuki H, Nakashima I: Arsenite induces apoptosis of murine T lymphocytes through membrane raft-linked signaling for activation of c-Jun amino-terminal kinase. J Immunol. 2000 Oct 15;165(8):4290-7. |
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| 10964950 | Namgung U, Xia Z: Arsenite-induced apoptosis in cortical neurons is mediated by c-Jun N-terminal protein kinase 3 and p38 mitogen-activated protein kinase. J Neurosci. 2000 Sep 1;20(17):6442-51. Here we investigated the role of JNK and p38 in cortical neuron apoptosis caused by sodium arsenite treatment. |
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| 12076508 | Hu Y, Jin X, Snow ET: Effect of arsenic on transcription factor AP-1 and NF-kappaB DNA binding activity and related gene expression. Toxicol Lett. 2002 Jul 7;133(1):33-45. Both acute (24 h) and chronic (10-20 week) exposure of human fibroblast cells to low dose sodium arsenite (As (III)) significantly affects activating protein-1 (AP-1) and nuclear factor kappa B (NF-kappa B) DNA binding activity. |
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| 12637567 | Kietzmann T, Samoylenko A, Immenschuh S: Transcriptional regulation of heme oxygenase-1 gene expression by MAP kinases of the JNK and p38 pathways in primary cultures of rat hepatocytes. J Biol Chem. 2003 May 16;278(20):17927-36. Epub 2003 Mar 11. Heme oxygenase-1 (HO-1) gene expression is induced by various oxidative stress stimuli including sodium arsenite. Electrophoretic mobility shift assays (EMSA) revealed that a CRE/AP-1 element (-668/-654) bound c-Jun, a target of the JNK pathway. |
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| 11325585 | Chevalier D, Thorin E, Allen BG: Simultaneous measurement of ERK, p38, and JNK MAP kinase cascades in vascular smooth muscle cells. J Pharmacol Toxicol Methods. 2000 Sep-Oct;44(2):429-39. Activation of the mitogen-activated protein kinase (MAP kinase) pathways in cultured porcine aortic vascular smooth muscle cells (VSMCs) was determined following a 5-min stimulation with endothelin-1 (ET-1), phorbol 12- 13- (PMA), H2O2, or sodium arsenite. The activation of these kinase cascades was also determined by resolving lysates on Mono Q using a fast protein liquid chromatography (FPLC) system and measuring the phosphorylation of specific substrates ERK1, c-Jun, and hsp27. |
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