| 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 | acrolein |
|---|---|
| CAS | 2-propenal |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12487375 | Ranganna K, Yousefipour Z, Nasif R, Yatsu FM, Milton SG, Hayes BE: Acrolein activates mitogen-activated protein kinase signal transduction pathways in rat vascular smooth muscle cells. Mol Cell Biochem. 2002 Nov;240(1-2):83-98. The extracellular signal-regulated kinases 1 and 2 (ERK1/2), stress-activated protein kinases/c-jun NH2-terminal kinases (SAPK/JNK) and p38MAPK are effectively and transiently activated by acrolein in a concentration and time-dependent fashion. |
162(2,2,2,2) | Details |
| 11329622 | Takeuchi K, Kato M, Suzuki H, Akhand AA, Wu J, Hossain K, Miyata T, Matsumoto Y, Nimura Y, Nakashima I: Acrolein induces activation of the epidermal growth factor receptor of human keratinocytes for cell death. J Cell Biochem. 2001;81(4):679-88. Selective phosphorylation/activation of EGFR followed by phosphorylation of MAP family kinases and c-Jun and their blockade by a specific EGFR inhibitor, AG1478, suggested that activation of EGFR is the major, and possibly single, cell surface element for intracellular signal transduction in acrolein-treated cells. |
32(0,1,1,2) | Details |
| 16337876 | Pugazhenthi S, Phansalkar K, Audesirk G, West A, Cabell L: Differential regulation of c-jun and CREB by acrolein and Free Radic Biol Med. 2006 Jan 1;40(1):21-34. Epub 2005 Sep 2. Acrolein and 4HNE increased the levels of active phosphorylated forms of c-jun and CREB, the transcription factors that promote apoptosis and cell survival, respectively. |
90(1,1,2,5) | Details |
| 10966506 | Kehrer JP, Biswal SS: The molecular effects of acrolein. . Toxicol Sci. 2000 Sep;57(1):6-15. It is apparent that the activation of the transcription factors nuclear factor kappa B (NF-kappa B) and activator protein 1 (AP-1) can be inhibited by acrolein. |
81(1,1,1,1) | Details |
| 17196791 | Tanel A, Averill-Bates DA: P38 and ERK mitogen-activated protein kinases mediate acrolein-induced apoptosis in Chinese hamster ovary cells. Cell Signal. 2007 May;19(5):968-77. Epub 2006 Nov 25. The MAP family kinases, including ERK and p38 kinase, and the transcription factor c-Jun were all activated by phosphorylation after 1 h exposure to acrolein. |
81(1,1,1,1) | Details |
| 11849044 | Biswal S, Acquaah-Mensah G, Datta K, Wu X, Kehrer JP: Inhibition of cell proliferation and AP-1 activity by acrolein in human A549 lung adenocarcinoma cells due to thiol imbalance and covalent modifications. Chem Res Toxicol. 2002 Feb;15(2):180-6. Inhibition of AP-1 activation also occurred following treatment with buthionine sulfoximine to deplete to the same extent as seen with acrolein. c-jun antisense treatments depressed c-jun protein below detectable levels at 4 h and inhibited cell proliferation (as assessed by [(3) H] incorporation) by 80%. |
37(0,1,2,2) | Details |
| 17225077 | Korkmaz A, Topal T, Oter S: Pathophysiological aspects of cyclophosphamide and ifosfamide induced hemorrhagic cystitis; implication of reactive and species as well as PARP activation. Cell Biol Toxicol. 2007 Sep;23(5):303-12. Epub 2007 Jan 15. Acrolein is the main molecule responsible of this side-effect and mesna (2-mercaptoethane sulfonate) is the commonly used preventive agent. Thus, many cytokines such as tumor necrosis factor (TNF) and the interleukin (IL) family and transcription factors such as nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) also play a role in its pathogenesis. |
1(0,0,0,1) | Details |
| 17510524 | Lee CW, Lee SH, Lee JW, Ban JO, Lee SY, Yoo HS, Jung JK, Moon DC, Oh KW, Hong JT: 2-hydroxycinnamaldehyde inhibits SW620 colon cancer cell growth through AP-1 inactivation. J Pharmacol Sci. 2007 May;104(1):19-28. In further studies on the mechanism, we found that consistent with the inhibitory effect on cell growth, HCA dose-dependently (0-20 microg/ml) inhibited DNA binding activity of AP-1 accompanied with down regulation of c-Jun and c-Fos expressions. |
1(0,0,0,1) | Details |
| 18972840 | Pokharel YR, Yoon SY, Kim SK, Li JD, Kang KW: Inhibition of acrolein-stimulated MUC5AC production by fucoidan in human bronchial epithelial cells. Pharmazie. 2008 Oct;63(10):757-9. The activation of both nuclear factor-kappa B (NF-kappa B) and activator protein 1 (AP-1) are key steps in the transcriptional activation of MUC5AC. |
1(0,0,0,1) | Details |
| 15064094 | Yang Y, Yang Y, Trent MB, He N, Lick SD, Zimniak P, Awasthi YC, Boor PJ: Glutathione-S-transferase A4-4 modulates oxidative stress in endothelium: possible role in human atherosclerosis. Atherosclerosis. 2004 Apr;173(2):211-21. Transfected cells demonstrated significantly higher GSTs enzyme activity and expressed significantly increased resistance to the cytotoxicity of allylamine, acrolein, (4-HNE), and H (2) O (2) (P < 0.05). Transfection protected MS1 endothelial cells from 4-HNE and H (2) O (2) induced apoptosis by inhibiting phosphorylation of c-Jun N-terminal kinases (p-JNK) and consequent activation of p53 and Bax. |
1(0,0,0,1) | Details |
| 19696094 | Conklin DJ, Haberzettl P, Lesgards JF, Prough RA, Srivastava S, Bhatnagar A: Increased sensitivity of glutathione S-transferase P-null mice to cyclophosphamide-induced urinary bladder toxicity. J Pharmacol Exp Ther. 2009 Nov;331(2):456-69. Epub 2009 Aug 20. Hemorrhagic cystitis and diffuse inflammation of the bladder, common side effects of cyclophosphamide (CY) treatment, have been linked to the generation of acrolein derived from CY metabolism. |
0(0,0,0,0) | Details |