| Name | mitogen activated protein kinase (protein family or complex) |
|---|---|
| Synonyms | MAPK; mitogen activated protein kinase; mitogen activated protein kinases |
| Name | carbon tetrachloride |
|---|---|
| CAS | tetrachloromethane |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16941698 | Zhang Y, Ikegami T, Honda A, Miyazaki T, Bouscarel B, Rojkind M, Hyodo I, Matsuzaki Y: Involvement of integrin-linked kinase in carbon tetrachloride-induced hepatic fibrosis in rats. J Biomed Sci. 2008 Mar;15(2):251-9. Epub 2007 Oct 6. Our studies also showed that ILK is involved in the phosphorylation of ERK 1/2, p38 MAPK, JNK, and PKB and that selective inhibition of ILK expression by siRNA results in a significant decrease in their phosphorylation. |
1(0,0,0,1) | Details |
| 20026116 | Dharancy S, Body-Malapel M, Louvet A, Berrebi D, Gantier E, Gosset P, Viala J, Hollebecque A, Moreno C, Philpott DJ, Girardin SE, Sansonetti PJ, Desreumaux P, Mathurin P, Dubuquoy L: Neutrophil migration during liver injury is under nucleotide-binding oligomerization domain 1 control. Gastroenterology. 2010 Apr;138(4):1546-56 Upon FK 565 stimulation, mitogen-activated protein kinase and nuclear factor kappaB were activated in Nod1 (+/+) PMNs, but less so in Nod1 (-/-) PMNs. METHODS: Nod1 (+/+) and Nod1 (-/-) mice were challenged with carbon tetrachloride (CCl (4)). |
1(0,0,0,1) | Details |
| 16527836 | Frelin L, Brenndorfer ED, Ahlen G, Weiland M, Hultgren C, Alheim M, Glaumann H, Rozell B, Milich DR, Bode JG, Sallberg M: The hepatitis C virus and immune evasion: non-structural 3/4A transgenic mice are resistant to lethal tumour necrosis factor alpha mediated liver disease. Gut. 2006 Oct;55(10):1475-83. Epub 2006 Mar 9. The TNFalpha resistance can be reverted by treatment with a p38 MAPK inhibitor. Liver damage was induced using carbon tetrachloride (CCl (4)), lipopolysaccaride (LPS), tumour necrosis factor alpha (TNFalpha), and anti-Fas antibody. |
1(0,0,0,1) | Details |
| 17032414 | Qiang H, Lin Y, Zhang X, Zeng X, Shi J, Chen YX, Yang MF, Han ZG, Xie WF: Differential expression genes analyzed by cDNA array in the regulation of rat hepatic fibrogenesis. Toxicology. 2007 Apr 11;232(3):200-15. Epub 2007 Jan 14. METHODS: Hepatic fibrosis was induced by intraperitoneal injection of dimethylnitrosamine or carbon tetrachloride (CCl (4)) injection subcutaneously in rats, and identification of the hepatic fibrosis related genes with cDNA microarray was performed. A total of 15 genes predominantly associated with the mitogen-activated protein kinase (MAPK) signal transduction pathway were upregulated in the fibrotic liver. |
1(0,0,0,1) | Details |
| 17869086 | Yun HS, Do SH, Jeong WI, Yang HJ, Yuan DW, Hong IH, Lee HR, Lee IS, Kim YK, Choi MS, Kim HA, Jeong KS: Cytotoxic effects of the isomers t10c12, c9t11-CLA and mixed form on rat hepatic stellate cells and CCl4-induced hepatic fibrosis. Hepatology. 2006 Sep;44(3):612-22. In order to evaluate the protective effect of CLA on carbon tetrachloride (CCl4)-induced hepatic fibrosis in vivo, animals were treated with 10% CCl4 to induce hepatic fibrosis during all experimental periods. |
0(0,0,0,0) | 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. |
82(1,1,1,2) | Details |
| 19567170 | Deng ZY, Li J, Jin Y, Chen XL, Lu XW: Effect of oxymatrine on the p38 mitogen-activated protein kinases signalling pathway in rats with CCl4 induced hepatic fibrosis. Eur J Pharmacol. 2007 Mar 22;559(2-3):115-23. Epub 2007 Jan 23. |
4(0,0,0,4) | Details |
| 17805973 | Pan Q, Zhang ZB, Zhang X, Shi J, Chen YX, Han ZG, Xie WF: Gene expression profile analysis of the spontaneous reversal of rat hepatic fibrosis by cDNA microarray. Lab Invest. 2007 Jun;87(6):591-601. Epub 2007 Mar 5. Expression of Mapk1 and Rps6ka1, which are critical members of the mitogen-activated protein kinase (MAPK) signaling pathway, was also investigated by Northern blot and immunohistochemistry. |
2(0,0,0,2) | Details |
| 17334410 | Hattori S, Dhar DK, Hara N, Tonomoto Y, Onoda T, Ono T, Yamanoi A, Tachibana M, Tsuchiya M, Nagasue N: FR-167653, a selective p38 MAPK inhibitor, exerts salutary effect on liver cirrhosis through downregulation of Runx2. Hepatology. 2008 Sep;48(3):909-19. In this study, we evaluated the salutary effect of FR-167653 (FR), a selective p38 inhibitor, in a carbon tetrachloride (CCl (4))-induced rat cirrhotic model. |
2(0,0,0,2) | Details |
| 18712785 | Nitta T, Kim JS, Mohuczy D, Behrns KE: Murine cirrhosis induces hepatocyte epithelial mesenchymal transition and alterations in survival signaling pathways. Gut. 2007 Jul;56(7):982-90. Epub 2006 Dec 21. Here, chronic murine liver injury was induced by twice-weekly carbon tetrachloride administration for 8 weeks. Normal liver-derived hepatocytes (NLDH) and cirrhotic liver-derived hepatocytes (CLDH) were examined for EMT and the small mothers against decapentaplegic homolog (Smad), phosphatidylinositol-3-kinase (PI3K/Akt), and mitogen activated protein kinase (MAPK) pathways were investigated. |
2(0,0,0,2) | Details |
| 18081878 | Fan Y, Shimizu T, Yamada T, Nanashima N, Akita M, Asano J, Tsuchida S: Development of glutathione S-transferase-P-negative foci accompanying nuclear factor-erythroid 2-related factor 2 expression during early stage of rat hepatocarcinogenesis. J Nutr Biochem. 2008 Mar;19(3):175-83. Epub 2007 Sep 14. After treatment with carbon tetrachloride, small vacuoles due to liver injury were frequently observed inside GST-P-negative foci but less frequently in GST-P-positive foci. In this study, we examined by immunohistochemistry whether JNK2, p38 mitogen-activated protein kinase, and Nrf2 were expressed in GST-P-positive foci induced by the Solt-Farber protocol. |
2(0,0,0,2) | 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. Chin Med J. 2009 Jun 20;122(12):1449-54. 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. |
1(0,0,0,1) | Details |
| 17298859 | Sawant SP, Dnyanmote AV, Mehendale HM: Mechanisms of inhibited liver tissue repair in toxicant challenged type 2 diabetic rats. 1556.e1-5. Epub 2009 Dec 21. In CCl (4)-treated non-diabetic (non-DB) rats, increased IL-6 levels, sustained activation of extracellular regulated kinases 1/2 (ERK1/2) MAPK, and sustained phosphorylation of retinoblastoma protein (p-pRB) via cyclin D1/cyclin-dependent kinase (cdk) 4 and cyclin D1/cdk6 complexes stimulated G (0)/G (1) to S-phase transition of liver cells. |
1(0,0,0,1) | Details |
| 17002867 | Farombi EO, Surh YJ: Heme oxygenase-1 as a potential therapeutic target for hepatoprotection. Liver Int. 2006 Nov;26(9):1126-37. 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 |
| 14980112 | Chen L, Sun HL, Yang L, Du HJ, An W: [Transfection of human hepatic stimulator substance gene could protect BEL-7402 cells against hepatotoxins]. Zhonghua Gan Zang Bing Za Zhi. 2004 Feb;12(2):99-101. MAPK phosphorylation was also activated after HSS transfected. |
1(0,0,0,1) | 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. Cancer Sci. 2008 Mar;99(3):497-501. Epub 2007 Dec 15. Bakuchiol treatment stimulated the activation of extracellular signal-regulated kinase 1/2 (ERK), c-Jun NH2-terminal protein kinase (JNK), and p38 mitogen-activated protein kinases (MAPK) in vitro. |
1(0,0,0,1) | Details |
| 17156884 | Fernandez-Varo G, Morales-Ruiz M, Ros J, Tugues S, Munoz-Luque J, Casals G, Arroyo V, Rodes J, Jimenez W: Impaired extracellular matrix degradation in aortic vessels of cirrhotic rats. J Hepatol. 2007 Mar;46(3):440-6. Epub 2006 Nov 13. Phosphorylated p38 MAPK and ERK1/2 were used to evaluate the activation of cell MAPK signaling pathways. |
1(0,0,0,1) | 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. J Biochem Mol Biol. 2006 Sep 30;39(5):479-91. C-jun (NH2) terminal kinase (JNK) is a member of the mitogen-activated protein kinase family and is a key intracellular signalling molecule involved in controlling the fate of cells. 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. |
1(0,0,0,1) | Details |
| 19066852 | Iida C, Fujii K, Koga E, Washino Y, Kitamura Y, Ichi I, Abe K, Matsura T, Kojo S: Effect of on carbon tetrachloride intoxication in the rat liver. Arch Toxicol. 2009 May;83(5):477-83. Epub 2008 Dec 10. The activation of JNK, ERK1/2 and p38 MAPK took place 1.5 h after CCl (4) administration. |
1(0,0,0,1) | Details |