| Name | JNK1 |
|---|---|
| Synonyms | Mitogen activated protein kinase 8; JNK 1; JNK 46; JNK1; JNK1 alpha protein kinase; JNK1 beta protein kinase; JNK1A2; JNK21B1/2… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 18218673 | Jin S, Ray RM, Johnson LR: TNF-alpha/cycloheximide-induced apoptosis in intestinal epithelial cells requires Rac1-regulated reactive species. Am J Physiol Gastrointest Liver Physiol. 2008 Apr;294(4):G928-37. Epub 2008 Jan 24. Previously we have shown that both Rac1 and c-Jun NH (2)-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-alpha/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive species (ROS) in apoptosis is unclear. |
33(0,1,1,3) | Details |
| 17916901 | Keum YS, Chang PP, Kwon KH, Yuan X, Li W, Hu L, Kong AN: 3-Morpholinopropyl isothiocyanate is a novel synthetic isothiocyanate that strongly induces the antioxidant response element-dependent Nrf2-mediated detoxifying/antioxidant enzymes in vitro and in vivo. Carcinogenesis. 2008 Mar;29(3):594-9. Epub 2007 Oct 4. Using chemical inhibitors of protein synthesis (cycloheximide) and 26S proteosomal degradation (MG-132), we observed that the induction of Nrf2 protein by 3MP-ITC appeared to be post-translationally regulated. 3MP-ITC activated ERK1/2 and JNK1/2 and the activation of antioxidant response element (ARE) by 3MP-ITC was significantly attenuated by chemical inhibition of PKC and PI3K signaling pathways in HepG2C8 cells. |
31(0,1,1,1) | Details |
| 16452486 | Seymour KJ, Roberts LE, Fini MA, Parmley LA, Oustitch TL, Wright RM: Stress activation of mammary epithelial cell xanthine oxidoreductase is mediated by p38 MAPK and CCAAT/enhancer-binding protein-beta. J Biol Chem. 2006 Mar 31;281(13):8545-58. Epub 2006 Feb 1. Activation of XOR gene expression by both cycloheximide and inflammatory cytokines suggested that XOR may be regulated by stress-activated protein kinases, the MAPKs. |
31(0,1,1,1) | Details |
| 17158707 | Bogoyevitch MA, Kobe B: Uses for JNK: the many and varied substrates of the c-Jun N-terminal kinases. Microbiol Mol Biol Rev. 2006 Dec;70(4):1061-95. JNKs were originally identified as stress-activated protein kinases in the livers of cycloheximide-challenged rats. |
6(0,0,1,1) | Details |
| 18439101 | Kato T, Noma H, Kitagawa M, Takahashi T, Oshitani N, Kitagawa S: Distinct role of c-Jun N-terminal kinase isoforms in human neutrophil apoptosis regulated by tumor necrosis factor-alpha and granulocyte-macrophage colony-stimulating factor. J Interferon Cytokine Res. 2008 Apr;28(4):235-43. The JNK isoforms phosphorylated by TNF-alpha and GM-CSF stimulation were found to be JNK1 and JNK2, respectively, on the basis of the molecular mass and the capture assay. TNF-alpha-induced JNK phosphorylation was sustained in the presence of cycloheximide, which was accompanied by accelerated neutrophil apoptosis. |
2(0,0,0,2) | Details |
| 16817231 | Siri S, Chen MJ, Chen TT: Biological activity of rainbow trout Ea4-peptide of the pro-insulin-like growth factor (pro-IGF)-I on promoting attachment of breast cancer cells (MDA-MB-231) via alpha2- and beta1-integrin. J Cell Biochem. 2006 Dec 15;99(6):1524-35. Expression of fibronectin 1 gene induced by rtEa4-peptide in MDA-MB-231 cells was abolished by inhibitors of PI3K, PKC, Mek1/2, JNK1/2, and p38 MAPK signaling transduction molecules. Blocking new protein synthesis by cycloheximide significantly reduced the attachment of MDA-MB-231 cells to rtEa4-peptide coated wells by 50%. |
2(0,0,0,2) | Details |
| 15956580 | Hargett D, McLean T, Bachenheimer SL: Herpes simplex virus ICP27 activation of stress kinases JNK and p38. . J Virol. 2005 Jul;79(13):8348-60. We previously reported that herpes simplex virus type 1 (HSV-1) can activate the stress-activated protein kinases (SAPKs) p38 and JNK. Cycloheximide reversal or treatment of wild-type virus-infected cells as well as infection with the ICP4 mutant vi13 indicated that only the immediate-early class of viral proteins were required for SAPK activation. |
1(0,0,0,1) | Details |
| 15557226 | Rahaus M, Desloges N, Wolff MH: Replication of varicella-zoster virus is influenced by the levels of JNK/SAPK and p38/MAPK activation. J Gen Virol. 2004 Dec;85(Pt 12):3529-40. Stimulation of the Jun NH (2)-terminal kinase/stress-activated protein kinase (JNK/SAPK) and the p38 mitogen-activated protein kinase (p38/MAPK) is part of the stress-related signal transduction pathways conveying signals from the cell surface into the nucleus in order to initiate programmes of gene expression. Blocking gene expression by treating cells with actinomycin D or cycloheximide prior to infection resulted in activation of neither JNK/SAPK nor p38/MAPK. |
1(0,0,0,1) | Details |
| 16339571 | Han B, Mura M, Andrade CF, Okutani D, Lodyga M, dos Santos CC, Keshavjee S, Matthay M, Liu M: TNFalpha-induced long pentraxin PTX3 expression in human lung epithelial cells via JNK. J Immunol. 2005 Dec 15;175(12):8303-11. Knockdown of either JNK1 or JNK2 with small interfering RNA also significantly reduced the regulated PTX3 expression. Pretreatment with either actinomycin D or cycloheximide abolished TNF-alpha-induced PTX3 expression, indicating the requirement for both transcriptional and translational regulation. |
1(0,0,0,1) | Details |
| 15714295 | Takatsume Y, Izawa S, Inoue Y: Unique regulation of glyoxalase I activity during osmotic stress response in the fission yeast Schizosaccharomyces pombe: neither the mRNA nor the protein level of glyoxalase I increase under conditions that enhance its activity. Arch Microbiol. 2005 Mar;183(3):224-7. Epub 2005 Feb 16. Cycloheximide blocked the induction of glyoxalase I activity in cells exposed to osmotic stress. In addition, glyoxalase I activity was increased in stress-activated protein kinase-deficient mutants (wis1 and spc1). |
1(0,0,0,1) | Details |
| 16158421 | Jin HO, Park IC, An S, Lee HC, Woo SH, Hong YJ, Lee SJ, Park MJ, Yoo DH, Rhee CH, Hong SI: Up-regulation of Bak and Bim via JNK downstream pathway in the response to in human glioblastoma cells. J Cell Physiol. 2006 Feb;206(2):477-86. In addition, de novo protein synthesis was required for the initiation of apoptosis in that the protein synthesis inhibitor, cycloheximide (CHX), inhibited NO-induced apoptotic cell death as well as up-regulation of Bak and Bim. |
0(0,0,0,0) | Details |
| 20339118 | Montezano AC, Burger D, Paravicini TM, Chignalia AZ, Yusuf H, Almasri M, He Y, Callera GE, He G, Krause KH, Lambeth D, Quinn MT, Touyz RM: Reduced Oxidase 5 (Nox5) Regulation by Angiotensin II and Endothelin-1 Is Mediated via /Calmodulin-Dependent, Rac-1-Independent Pathways in Human Endothelial Cells. Circ Res. 2010 Mar 25. Effects were inhibited by actinomycin D and cycloheximide and blunted by calmidazolium and low extracellular Ca (2+) ([Ca (2+)] e). |
0(0,0,0,0) | Details |