| 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 | carbon tetrachloride |
|---|---|
| CAS | tetrachloromethane |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17728180 | Aoyama C, Ishidate K, Sugimoto H, Vance DE: Induction of choline kinase alpha by carbon tetrachloride (CCl4) occurs via increased binding of c-jun to an AP-1 element. Biochim Biophys Acta. 2007 Sep;1771(9):1148-55. Epub 2007 Jul 24. |
84(1,1,1,4) | Details |
| 16393475 | Lee SJ, Oh PS, Ko JH, Lim K, Lim KT: Protective effect of glycoprotein isolated from Ulmus davidiana Nakai on carbon tetrachloride-induced mouse liver injury. J Pharm Pharmacol. 2006 Jan;58(1):143-52. We evaluated lipid peroxidation in / oxidase (G/GO)-induced BNL CL.2 cells and measured thiobarbituric acid reactive substances (TBARS), lactate dehydrogenase (LDH), (NO), antioxidant enzyme (superoxide dismutase (SOD), catalase (CAT) and peroxidase (GPx)), activity of cytotoxic-related signals (hepatic cytochrome c, nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1)) and levels of plasma lipids (triglyceride (TG) and total (TC)) in carbon tetrachloride (CCl (4,) 1.0 mL kg (-1))-induced A/J mouse. |
6(0,0,1,1) | Details |
| 15760680 | Sudo K, Yamada Y, Moriwaki H, Saito K, Seishima M: Lack of tumor necrosis factor receptor type 1 inhibits liver fibrosis induced by carbon tetrachloride in mice. Cytokine. 2005 Mar 7;29(5):236-44. Furthermore, a marked reduction in procollagen and TGF-beta synthesis was observed in TNFR-1 KO mice, which also had little detectable NF-kappa B, STAT3, and AP1 binding, and reduced levels of liver interleukin-6 (IL-6) mRNA compared to WT and TNFR-2 KO mice. |
2(0,0,0,2) | Details |
| 17292878 | Park EJ, Zhao YZ, Kim YC, Sohn DH: Bakuchiol-induced caspase-3-dependent apoptosis occurs through c-Jun NH2-terminal kinase-mediated mitochondrial translocation of Bax in rat liver myofibroblasts. Eur J Pharmacol. 2007 Mar 22;559(2-3):115-23. Epub 2007 Jan 23. |
2(0,0,0,2) | Details |
| 17185352 | Henderson NC, Pollock KJ, Frew J, Mackinnon AC, Flavell RA, Davis RJ, Sethi T, Simpson KJ: Critical role of c-jun (NH2) terminal kinase in - induced acute liver failure. Gut. 2007 Jul;56(7):982-90. Epub 2006 Dec 21. JNK inhibition was not protective in acute carbon tetrachloride-mediated or anti-Fas antibody-mediated hepatic injury, suggesting specificity for the role of JNK in hepatotoxicity. |
2(0,0,0,2) | Details |
| 17285312 | Iida C, Fujii K, Kishioka T, Nagae R, Onishi Y, Ichi I, Kojo S: Activation of mitogen activated protein kinase (MAPK) during carbon tetrachloride intoxication in the rat liver. Arch Toxicol. 2007 Jul;81(7):489-93. Epub 2007 Feb 7. Phosphorylated JNK (c-Jun NH (2)-terminal kinase) and phospho-ERK1/2 (extracellular signal-regulated kinase1/2) were significantly increased transiently 1-3 h after treatment with CCl (4), while phosphorylated p38 decreased significantly 1-24 h after CCl (4) treatment. |
1(0,0,0,1) | Details |
| 17002867 | Farombi EO, Surh YJ: Heme oxygenase-1 as a potential therapeutic target for hepatoprotection. J Biochem Mol Biol. 2006 Sep 30;39(5):479-91. Advances in unveiling signal transduction network indicate that a battery of redox-sensitive transcription factors, such as activator protein-1 (AP-1), nuclear factor-kappa B (NF-kappaB) and nuclear factor E2-related factor-2 (Nrf2), and their upstream kinases including mitogen-activated protein kinases play an important regulatory role in HO-1 gene induction. In this context, it is interesting to note that induction of HO-1 expression contributes to protection against liver damage induced by several chemical compounds such as carbon tetrachloride and heavy metals, suggesting HO-1 induction as an important cellular endeavor for hepatoprotection. |
1(0,0,0,1) | Details |
| 16823256 | Ko JH, Lim KT: Glycoprotein isolated from Ulmus davidiana NAKAI protects against carbon tetrachloride-induced liver injury in the mouse. J Pharmacol Sci. 2006 Jul;101(3):205-13. Epub 2006 Jul 6. In addition, UDN glycoprotein increased the production and decreased the nuclear factor-kappa B and activator protein-1 activation in CCl4-treated mice. |
1(0,0,0,1) | Details |
| 16904936 | Li W, Zhang J, Huang Q, Zhu H, Zhang X: Long-term administering low anticoagulant activity can lessen rat hepatic fibrosis induced by either CCl (4) or porcine serum injection. Hepatol Res. 2006 Oct;36(2):115-23. Epub 2006 Aug 14. Activator protein-1 (AP-1) activity in nuclear proteins of HSCs was measured by the electrophoresis motility shift assay (EMSA). We are here demonstrating by both biochemical and morphological methods that long term LAAH administering can considerably decrease the hepatic fibrosis in rats elicited by carbon tetrachloride (CCl (4)) or injection of porcine serum. |
1(0,0,0,1) | Details |
| 17002669 | Lee SJ, Oh PS, Lim KT: Hepatoprotective and hypolipidaemic effects of glycoprotein isolated from Gardenia jasminoides ellis in mice. Clin Exp Pharmacol Physiol. 2006 Oct;33(10):925-33. In addition, in these mice GJE resulted in increased production and the activation of anti-oxidant enzymes, accompanied by the inhibition of the cytotoxic-related signals hepatic cytochrome c, nuclear factor-kappaB and activator protein-1. |
1(0,0,0,1) | Details |
| 20093790 | Kim HY, Kim JK, Choi JH, Jung JY, Oh WY, Kim DC, Lee HS, Kim YS, Kang SS, Lee SH, Lee SM: Hepatoprotective effect of pinoresinol on carbon tetrachloride-induced hepatic damage in mice. J Pharmacol Sci. 2010 Jan;112(1):105-12. Nuclear translocation of nuclear factor-kappaB (NF-kappaB) and phosphorylation of c-Jun, one of the components of activating protein 1 (AP-1), were inhibited by pinoresinol. |
1(0,0,0,1) | Details |
| 18429990 | Leung TM, Tipoe GL, Liong EC, Lau TY, Fung ML, Nanji AA: Endothelial nitric oxide synthase is a critical factor in experimental liver fibrosis. Int J Exp Pathol. 2008 Aug;89(4):241-50. Epub 2008 Apr 21. Chronic liver injury was induced by administration of carbon tetrachloride (CCl (4)) to mice for 8 weeks. 5-Methylisothiourea hemisulphate (SMT), an iNOS inhibitor, or a NOS substrate were injected subcutaneously. The expression levels of inducible NOS (iNOS) and nuclear factor kappa-B (NF-kappaB) activity in the liver after CCl (4) treatment were increased but eNOS expression and activator protein-1 (AP-1) activity were decreased. |
1(0,0,0,1) | Details |
| 15027814 | Chan WY, Chau FT, Lee KK, Kwong WH, Yew DT: Substitution for natural musk in Pien Tze Huang does not affect its hepatoprotective activities. Hum Exp Toxicol. 2004 Jan;23(1):35-47. Previous studies showed that Pien Tze Huang, a Chinese folk medicine well known for its therapeutic activity in treating liver diseases, protected the liver against carbon tetrachloride (CCl4)-induced damage in mice. In hepatoma cells, both formulations activated the activator protein 1 (AP1) enhancer sequence, indicating that both of them were able to act through the JNK signal transduction pathway. |
1(0,0,0,1) | Details |