| Name | AP 1 (protein family or complex) |
|---|---|
| Synonyms | AP 1; AP 1 complex; AP1; Adapter related protein complex 1 |
| 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. |
83(1,1,1,3) | 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 |
| 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. 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. And its inhibition of fibrosis may be associated with the intervention of ERK signal transduction pathway and down-regulation of AP-1 activity in hepatic stellate cells. |
4(0,0,0,4) | Details |
| 17009398 | Salazar-Montes A, Ruiz-Corro L, Sandoval-Rodriguez A, Lopez-Reyes A, Armendariz-Borunda J: Increased DNA binding activity of NF-kappaB, STAT-3, SMAD3 and AP-1 in acutely damaged liver. World J Gastroenterol. 2006 Oct 7;12(37):5995-6001. |
3(0,0,0,3) | 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. |
3(0,0,0,3) | Details |
| 20056141 | Lou JL, Jiang MN, Li C, Zhou Q, He X, Lei HY, Li J, Jia YJ: Herb medicine Gan-fu-kang attenuates liver injury in a rat fibrotic model. J Ethnopharmacol. 2010 Mar 2;128(1):131-8. Epub 2010 Jan 6. MATERIALS AND METHODS: Liver fibrosis was established by 12 weeks of carbon tetrachloride (CCl (4)) treatment (0.5mg/kg, twice per week) followed by 8 weeks of "recovery" in rats. RESULTS AND CONCLUSIONS: (1) CCl (4) treatment resulted in severe liver damage and fibrosis. (2) In the main block of the 20-week study, GFK attenuated liver damage and fibrosis. (3) In the 12-week study, GFK produced prevention effect against hepatic injury. (4) GFK suppressed the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), type I collagen, platelet-derived growth factor-BB (PDGF-BB)/PDGF receptor-beta chains (PDGFRbeta) and mitogen-activated protein kinases (MAPKs)/active protein-1 (AP-1) signal pathways. |
2(0,0,0,2) | 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. |
2(0,0,0,2) | 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 |
| 15261760 | Taniguchi M, Takeuchi T, Nakatsuka R, Watanabe T, Sato K: Molecular process in acute liver injury and regeneration induced by carbon tetrachloride. Life Sci. 2004 Aug 13;75(13):1539-49. Down-regulation of liver-specific genes was accomplished through suppression of liver-enriched transcription factors and box A factors found in the catalase gene, and induction of NF-kappaB, AP-1 and a novel factor denoted as 'cx' in the catalase gene. |
1(0,0,0,1) | Details |
| 17584048 | Tipoe GL, Leung TM, Hung MW, Fung ML: Green tea polyphenols as an anti-oxidant and anti-inflammatory agent for cardiovascular protection. Cardiovasc Hematol Disord Drug Targets. 2007 Jun;7(2):135-44. can also reduce the inflammatory response associated with local tissue injuries such as the hepatocellular necrosis in acute liver injury induced by carbon tetrachloride. |
0(0,0,0,0) | Details |