| Name | Bcl xL |
|---|---|
| Synonyms | Apoptosis regulator Bcl X; BCL XL/S; BCL2 like 1; BCL2 related gene; BCL2 like 1 isoform 1; BCL2L; BCL2L1; BCLX… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17200126 | Adams KW, Cooper GM: Rapid turnover of mcl-1 couples translation to cell survival and apoptosis. J Biol Chem. 2007 Mar 2;282(9):6192-200. Epub 2007 Jan 2. Caspase inhibition and overexpression of Bcl-x (L) blocked cycloheximide-induced apoptosis. |
81(1,1,1,1) | Details |
| 19665696 | Oguma T, Ono T, Kajiwara T, Sato M, Miyahira Y, Arino H, Yoshihara Y, Tadakuma T: CD4 (+) CD8 (+) thymocytes are induced to cell death by a small dose of puromycin via ER stress. Cell Immunol. 2009;260(1):21-7. Epub 2009 Jul 14. The induction of apoptosis was blocked by the protein synthesis inhibitor cycloheximide, and to some extent by transfection of Bcl-xL or Bcl-2 genes. |
31(0,1,1,1) | Details |
| 19003387 | Charbonneau JR, Gauthier ER: Prolongation of murine hybridoma cell survival in stationary batch culture by Bcl-xL expression. Cytotechnology. 2000 Oct;34(1-2):131-9. This murine hybridomaexpresses low levels of Bcl-xL and is highly sensitiveto apoptosis induction by cycloheximide (CHX) and byamino acid depletion. |
12(0,0,1,7) | Details |
| 18096507 | Boon-Unge K, Yu Q, Zou T, Zhou A, Govitrapong P, Zhou J: Emetine regulates the alternative splicing of Bcl-x through a protein phosphatase 1-dependent mechanism. Chem Biol. 2007 Dec;14(12):1386-92. |
4(0,0,0,4) | Details |
| 19439449 | Zhang Y, Xing D, Liu L: PUMA promotes Bax translocation by both directly interacting with Bax and by competitive binding to Bcl-X L during UV-induced apoptosis. Mol Biol Cell. 2009 Jul;20(13):3077-87. Epub 2009 May 13. In addition, pifithrin-alpha (a p53 inhibitor) and cycloheximide (a protein synthesis inhibitor) could inhibit PUMA-mediated Bax translocation and cell apoptosis. |
4(0,0,0,4) | Details |
| 15653751 | Bosque A, Pardo J, Martinez-Lorenzo MJ, Iturralde M, Marzo I, Pineiro A, Alava MA, Naval J, Anel A: Down-regulation of normal human T cell blast activation: roles of APO2L/TRAIL, FasL, and c- FLIP, Bim, or Bcl-x isoform expression. J Leukoc Biol. 2005 Apr;77(4):568-78. Epub 2005 Jan 14. Cell death was only observed in the presence of cycloheximide or after a pulse through CD3 or CD59, correlating with a net reduction in cellular Fas-associated death domain-like IL-1beta-converting enzyme-inhibitory protein long (c-FLIPL) and c-FLIPS expression. |
3(0,0,0,3) | Details |
| 19002913 | Charbonneau J, Gauthier E: Protection of hybridoma cells against apoptosis by a loop domain-deficient Bcl-xL protein. Cytotechnology. 2001 Sep;37(1):41-7. In contrast, protection against the cytotoxic effects of cycloheximide (CHX) was highly dependent on the level of expression of the Bcl-xLtriangle up 46-83 mutant. |
3(0,0,0,3) | Details |
| 18657356 | Wu Y, Xing D, Liu L, Gao B: Regulation of Bax activation and apoptotic response to UV irradiation by p53 transcription-dependent and -independent pathways. Cancer Lett. 2008 Nov 28;271(2):231-9. Epub 2008 Jul 25. Then using CHX (cycloheximide) to prevent new protein expression in response to p53, we also find that Bax translocation and cell death by UV irradiation are delayed. Furthermore we find that overexpression of Bcl-x (L), an inhibitor of cytoplasmic p53 after UV irradiation, prevents cell death. |
2(0,0,0,2) | Details |
| 20017956 | Cho SH, Chung KS, Choi JH, Kim DH, Lee KT: Compound K, a metabolite of ginseng saponin, induces apoptosis via caspase-8-dependent pathway in HL-60 human leukemia cells. BMC Cancer. 2009 Dec 18;9:449. Interestingly, the activation of caspase-3 and -8 and DNA fragmentation were significantly prevented in the presence of cycloheximide, suggesting that Compound K-induced apoptosis is dependent on de novo protein synthesis. In addition, compound-K induced a series of intracellular events associated with both the mitochondrial- and death receptor-dependent apoptotic pathways, namely, (1) the activation of caspases-3, -8, and -9; (2) the loss of mitochondrial membrane potential; (3) the release of cytochrome c and Smac/DIABLO to the cytosol; (4) the translocation of Bid and Bax to mitochondria; and (5) the downregulations of Bcl-2 and Bcl-xL. |
1(0,0,0,1) | Details |
| 18690848 | Clark DW, Mitra A, Fillmore RA, Jiang WG, Samant RS, Fodstad O, Shevde LA: NUPR1 interacts with p53, transcriptionally regulates p21 and rescues breast epithelial cells from doxorubicin-induced genotoxic stress. Curr Cancer Drug Targets. 2008 Aug;8(5):421-30. Since NUPR1 upregulated p21, concomitant with phosphorylation of Rb and upregulation of the anti-apoptotic protein, Bcl-x (L) we propose that NUPR1 expression imparts a cell growth and survival advantage. An increase in NUPR1 expression has been seen with serum starvation and in response to compounds such as cycloheximide, and staurosporine. |
1(0,0,0,1) | Details |
| 15637055 | Weng C, Li Y, Xu D, Shi Y, Tang H: Specific cleavage of Mcl-1 by caspase-3 in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in Jurkat leukemia T cells. J Biol Chem. 2005 Mar 18;280(11):10491-500. Epub 2005 Jan 6. In sharp contrast to cycloheximide-induced Mcl-1 dilapidation, TRAIL did not activate proteasomal degradation of Mcl-1 in Jurkat cells. |
0(0,0,0,0) | Details |
| 17575110 | Liu T, Hannafon B, Gill L, Kelly W, Benbrook D: Flex-Hets differentially induce apoptosis in cancer over normal cells by directly targeting mitochondria. Mol Cancer Ther. 2007 Jun;6(6):1814-22. Inhibition of protein synthesis with cycloheximide also did not prevent Flex-Het mitochondrial or apoptosis effects. Bcl-2, Bcl-x (L), and Bax were measured by Western blot. |
2(0,0,0,2) | Details |
| 17641050 | Wang HL, Akinci IO, Baker CM, Urich D, Bellmeyer A, Jain M, Chandel NS, Mutlu GM, Budinger GR: The intrinsic apoptotic pathway is required for lipopolysaccharide-induced lung endothelial cell death. J Immunol. 2007 Aug 1;179(3):1834-41. We sought to determine whether LPS and cycloheximide-induced cell death in human lung microvascular endothelial cells (HmVECs) was dependent upon activation of the intrinsic apoptotic pathway and the generation of reactive species. We found that cells overexpressing the anti-apoptotic protein Bcl-X (L) were resistant to LPS and cycloheximide-induced death and that the proapoptotic Bcl-2 protein Bid was cleaved following treatment with LPS. |
1(0,0,0,1) | Details |
| 15670574 | Kadohara K, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Acetoxycycloheximide (E-73) rapidly induces apoptosis mediated by the release of cytochrome c via activation of c-Jun N-terminal kinase. Biochem Pharmacol. 2005 Feb 15;69(4):551-60. Epub 2004 Dec 28. Cycloheximide (CHX) is an inhibitor of protein synthesis and commonly used to modulate death receptor-mediated apoptosis or to induce apoptosis in a number of normal and transformed cells. The Bcl-2 family protein Bcl-x (L) suppressed cytochrome c release as well as processing of procaspases-3, -8, and -9 in E-73-treated cells. |
1(0,0,0,1) | Details |
| 16260615 | Ohgushi M, Kuroki S, Fukamachi H, O'Reilly LA, Kuida K, Strasser A, Yonehara S: Transforming growth factor beta-dependent sequential activation of Smad, Bim, and caspase-9 mediates physiological apoptosis in gastric epithelial cells. Mol Cell Biol. 2005 Nov;25(22):10017-28. In addition, treatment with TGF-beta induced binding of Bim, a proapoptotic Bcl-2 homology domain 3 (BH3)-only protein, to Bcl-X (L), which is dependent on the activation of Smad, and reduction in the expression of Bim by RNA interference decreased the sensitivity to TGF-beta-induced apoptosis. |
1(0,0,0,1) | Details |
| 19372210 | Li TW, Zhang Q, Oh P, Xia M, Chen H, Bemanian S, Lastra N, Circ M, Moyer MP, Mato JM, Aw TY, Lu SC: and inhibit cellular FLICE inhibitory protein expression and induce apoptosis in colon cancer cells. Mol Pharmacol. 2009 Jul;76(1):192-200. Epub 2009 Apr 16. and MTA are also proapoptotic in liver cancer cells by selectively inducing Bcl-x (S) expression. |
1(0,0,0,1) | Details |
| 16133866 | Drexler HC, Euler M: Synergistic apoptosis induction by proteasome and histone deacetylase inhibitors is dependent on protein synthesis. Apoptosis. 2005 Aug;10(4):743-58. Apoptosis was also delayed by overexpression of Bcl-xL, as well as by crmA, a known inhibitor of caspases 1 and 8. The most striking anti-apoptotic effect though was obtained by the translational inhibitor cycloheximide, which abolished caspase 8 processing, blocked Bid cleavage and maintained the mitochondrial transmembrane potential. |
1(0,0,0,1) | Details |
| 15542778 | Doi S, Soda H, Oka M, Tsurutani J, Kitazaki T, Nakamura Y, Fukuda M, Yamada Y, Kamihira S, Kohno S: The histone deacetylase inhibitor FR901228 induces caspase-dependent apoptosis via the mitochondrial pathway in small cell lung cancer cells. Mol Cancer Ther. 2004 Nov;3(11):1397-402. FR901228 down-regulated the expression of bcl-2 and bcl-xL mRNA through de novo protein synthesis and suppressed the expression of BCL-2 and BCL-XL proteins. |
1(0,0,0,1) | Details |
| 19136059 | Bhattacharya S, Ray RM, Johnson LR: Role of polyamines in p53-dependent apoptosis of intestinal epithelial cells. Cell Signal. 2009 Apr;21(4):509-22. Epub 2008 Dec 24. The translation inhibitor, cycloheximide (CHX), prevented CPT-induced apoptosis. CHX completely prevented CPT-induced p53 phosphorylation and synthesis of p21Cip1, Bax and Bcl-xL proteins without altering p53 levels. |
1(0,0,0,1) | Details |
| 18234961 | Chetoui N, Sylla K, Gagnon-Houde JV, Alcaide-Loridan C, Charron D, Al-Daccak R, Aoudjit F: Down-regulation of mcl-1 by small interfering RNA sensitizes resistant melanoma cells to fas-mediated apoptosis. Mol Cancer Res. 2008 Jan;6(1):42-52. In this study, we report that treatment of Fas-resistant melanoma cell lines with cycloheximide, a general inhibitor of de novo protein synthesis, sensitizes them to anti-Fas monoclonal antibody (mAb)-induced apoptosis. |
0(0,0,0,0) | Details |
| 16581346 | Tamai M, Kawakami A, Tanaka F, Miyashita T, Nakamura H, Iwanaga N, Izumi Y, Arima K, Aratake K, Huang M, Kamachi M, Ida H, Origuchi T, Eguchi K: Significant inhibition of TRAIL-mediated fibroblast-like synovial cell apoptosis by IFN-gamma through JAK/STAT pathway by translational regulation. J Lab Clin Med. 2006 Apr;147(4):182-90. Janus kinase (JAK)-induced phosphorylation of STAT1/3/6, which acts at translational regulation, seemed to be crucial because chemical inhibition of JAK as well as cycloheximide (CHX) abolished both the phosphorylation of STAT1/3/6 and the IFN-gamma-induced inhibitory effect. |
0(0,0,0,0) | Details |