| Name | p38 |
|---|---|
| Synonyms | AIMP 2; p38; AIMP2; JTV 1; JTV1; JTV1 gene; JTV1 protein; Multisynthetase complex auxiliary component p38… |
| Name | carbon tetrachloride |
|---|---|
| CAS | tetrachloromethane |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. Cancer Sci. 2008 Mar;99(3):497-501. Epub 2007 Dec 15. 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. |
3(0,0,0,3) | Details |
| 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. Hepatology. 2006 Sep;44(3):612-22. 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 |
| 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 |
| 18753413 | Khimji AK, Shao R, Rockey DC: Divergent transforming growth factor-beta signaling in hepatic stellate cells after liver injury: functional effects on ECE-1 regulation. Am J Pathol. 2008 Sep;173(3):716-27. We measured Smad3 and MAP kinase activation after isolating stellate cells from rat livers injured by either bile duct ligation (BDL) or repeated carbon tetrachloride (CCl (4)) administration. TGF-beta signaling in stellate cells activated after BDL was mediated prominently through ERK activation, whereas activation induced by CCl (4) injury or culture led to a cross-signaling mechanism involving both Smad3 and p38. |
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 |
| 20203062 | von Montfort C, Beier JI, Kaiser JP, Guo L, Joshi-Barve S, Pritchard MT, States JC, Arteel GE: PAI-1 plays a protective role in CCl4-induced hepatic fibrosis in mice: role of hepatocyte division. Am J Physiol Gastrointest Liver Physiol. 2010 Mar 4. Under these conditions, a decrease in phospho-p38, coupled with elevated p53 protein, was observed; these results suggest impaired proliferation and a potential G (1)/S cell cycle arrest in PAI-1 (-/-) mice. However, its role in more severe models of hepatic fibrosis (e.g., carbon tetrachloride; CCl (4)) has not been determined and is important for extrapolation to human disease. |
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. Eur J Pharmacol. 2007 Mar 22;559(2-3):115-23. Epub 2007 Jan 23. 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 |
| 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 |
| 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. Lab Invest. 2007 Jun;87(6):591-601. Epub 2007 Mar 5. 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. |
36(0,1,1,6) | 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. Chin Med J. 2009 Jun 20;122(12):1449-54. |
5(0,0,0,5) | Details |