| Name | bcl 2 |
|---|---|
| Synonyms | Apoptosis regulator Bcl 2; B cell CLL/lymphoma 2; B cell lymphoma protein 2 alpha; B cell lymphoma protein 2 alpha isoform; BCL2; Bcl 2; B cell CLL/lymphoma 2s; B cell lymphoma protein 2 alphas… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19151744 | Liu HY, Wang ZM, Bai Y, Wang M, Li Y, Wei S, Zhou QH, Chen J: Different BAG-1 isoforms have distinct functions in modulating chemotherapeutic-induced apoptosis in breast cancer cells. Acta Pharmacol Sin. 2009 Feb;30(2):235-41. Epub 2009 Jan 19. The mechanism by which BAG-1 affected the function of Bcl-2 was exploredby using the cycloheximide chase assay. |
163(2,2,2,3) | 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. Our finding on the regulation of RNA splicing of members of the Bcl-2 family in response to emetine presents a potential target for cancer treatment. |
1(0,0,0,1) | 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. The Trp53 tumor suppressor gene product (p53) functions in the nucleus to regulate proapoptotic genes, whereas cytoplasmic p53 directly activates proapoptotic Bcl-2 proteins to permeabilize mitochondria and initiate apoptosis. 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. |
1(0,0,0,1) | Details |
| 19777442 | Pucci B, Indelicato M, Paradisi V, Reali V, Pellegrini L, Aventaggiato M, Karpinich NO, Fini M, Russo MA, Farber JL, Tafani M: ERK-1 MAP kinase prevents TNF-induced apoptosis through bad phosphorylation and inhibition of Bax translocation in HeLa Cells. J Cell Biochem. 2009 Dec 1;108(5):1166-74. Extracellular signal-regulated kinase (ERK) 1/2 signaling is involved in tumor cell survival through the regulation of Bcl-2 family members. |
1(0,0,0,1) | Details |
| 19347031 | Ciechomska IA, Goemans GC, Skepper JN, Tolkovsky AM: Bcl-2 complexed with Beclin-1 maintains full anti-apoptotic function. . Oncogene. 2009 May 28;28(21):2128-41. Epub 2009 Apr 6. We targeted Bcl-2 to mitochondria or endoplasmic reticulum (ER) and induced apoptosis using several apoptotic stimuli that initiate ER and/or mitochondrial signaling pathways (UV radiation, TNF and cycloheximide, staurosporine, thapsigargin and tunicamycin). |
35(0,1,1,5) | Details |
| 19412536 | Robert F, Carrier M, Rawe S, Chen S, Lowe S, Pelletier J: Altering chemosensitivity by modulating translation elongation. PLoS One. 2009;4(5):e5428. Epub 2009 May 1. METHODOLOGY/PRINCIPAL FINDINGS: Here, we chose four structurally different chemical inhibitors of translation elongation: homoharringtonine, bruceantin, didemnin B and cycloheximide, and tested their ability to alter the chemoresistance of Emu-myc lymphomas harbouring lesions in Pten, Tsc2, Bcl-2, or eIF4E. |
31(0,1,1,1) | Details |
| 15754039 | Lai MD, Lin WC, Sun YM, Chang FL: Phosphorylated and hypoacetylated mutant p53 enhances cisplatin-induced apoptosis through caspase-9 pathway in the absence of transcriptional activation or translation. Int J Mol Med. 2005 Apr;15(4):725-34. Both transcriptional inhibitor actinomycin D and translational inhibitor cycloheximide did not inhibit apoptosis. Transcriptional repression of Bcl-2 occurred during apoptosis and could be reversed by the treatment of histone deacetylase inhibitor trichostatin A (TSA). |
1(0,0,0,1) | Details |
| 16956375 | Leak RK, Liou AK, Zigmond MJ: Effect of sublethal on the response to subsequent oxidative stress in dopaminergic cells: evidence for preconditioning. J Neurochem. 2006 Nov;99(4):1151-63. Epub 2006 Sep 4. The antioxidant, N-acetyl (20 mM), when applied during preconditioning, abolished protection, as did the protein synthesis inhibitor, cycloheximide (0.2 microM). However, Bcl-2 protein levels rose with preconditioning. |
1(0,0,0,1) | 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 |
| 18977202 | Nakashima T, Tanaka R, Yamashita Y, Kanda Y, Hara M: Aranorosin and a novel derivative inhibit the anti-apoptotic functions regulated by Bcl-2. Biochem Biophys Res Commun. 2008 Dec 26;377(4):1085-90. Epub 2008 Oct 31. |
7(0,0,0,7) | Details |
| 17516030 | Yun X, Wu Y, Yao L, Zong H, Hong Y, Jiang J, Yang J, Zhang Z, Gu J: CDK11 (p58) protein kinase activity is associated with Bcl-2 down-regulation in pro-apoptosis pathway. Mol Cell Biochem. 2007 Oct;304(1-2):213-8. Epub 2007 May 22. Our previous study proved that CDK11 (p58)-enhanced cycloheximide (CHX)-induced apoptosis in SMMC-7721 hepatocarcinoma cells. |
5(0,0,0,5) | Details |
| 18064628 | Espina B, Liang M, Russell RG, Hulley PA: Regulation of bim in glucocorticoid-mediated osteoblast apoptosis. J Cell Physiol. 2008 May;215(2):488-96. We found dose- and time-dependent upregulation of Bim protein, a pro-apoptotic Bcl-2 family member, with highest levels at 24-48 h for 1 microM Dex. Bim mRNA was upregulated in response to 1 microM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex-induction of Bim protein, indicating transcriptional regulation involving the GC receptor. |
1(0,0,0,1) | Details |
| 16598301 | Lu Y, Xu YB, Yuan TT, Song MG, Lubbert M, Fliegauf M, Chen GQ: Inducible expression of AML1-ETO fusion protein endows leukemic cells with susceptibility to extrinsic and intrinsic apoptosis. Leukemia. 2006 Jun;20(6):987-93. We show that AML1-ETO significantly stabilizes death receptor Fas protein and increases proapoptotic Bak in addition to reducing Bcl-2 expression. |
1(0,0,0,1) | Details |
| 18252892 | McKenzie MD, Carrington EM, Kaufmann T, Strasser A, Huang DC, Kay TW, Allison J, Thomas HE: Proapoptotic BH3-only protein Bid is essential for death receptor-induced apoptosis of pancreatic beta-cells. Diabetes. 2008 May;57(5):1284-92. Epub 2008 Feb 5. The role in these processes of pro- and antiapoptotic Bcl-2 family proteins, which regulate apoptosis by controlling mitochondrial integrity, remains poorly understood. Bid-deficient islets were also resistant to apoptosis induced by TNF-alpha plus cycloheximide and were partially resistant to proinflammatory cytokine-induced death. |
4(0,0,0,4) | Details |
| 17245642 | Chen SP, Wu JL, Su YC, Hong JR: Anti-Bcl-2 family members, zfBcl-x (L) and zfMcl-1a, prevent cytochrome c release from cells undergoing betanodavirus-induced secondary necrotic cell death. Apoptosis. 2007 Jun;12(6):1043-60. To identify the mediator (s) of this necrotic process, a protein synthesis inhibitor (cycloheximide; CHX; 0.33 microg/ml) was used to block cytochrome c release as well as PS exposure and mitochondrial membrane permeability transition pore (MMP) loss. |
3(0,0,0,3) | Details |
| 17955372 | Lin PW, Huang YJ, John JA, Chang YN, Yuan CH, Chen WY, Yeh CH, Shen ST, Lin FP, Tsui WH, Chang CY: Iridovirus Bcl-2 protein inhibits apoptosis in the early stage of viral infection. Apoptosis. 2008 Jan;13(1):165-76. Northern blot hybridization showed that GIV-Bcl transcription began at 2 h post-infection, and the mRNA level significantly increased in the presence of cycloheximide or aphidicolin, indicating that this GIV-Bcl is an immediate-early gene. |
3(0,0,0,3) | Details |
| 19264808 | Wickramasinghe NS, Manavalan TT, Dougherty SM, Riggs KA, Li Y, Klinge CM: downregulates miR-21 expression and increases miR-21 target gene expression in MCF-7 breast cancer cells. Nucleic Acids Res. 2009 May;37(8):2584-95. Epub 2009 Mar 5. The E (2)-mediated decrease in miR-21 correlated with increased protein expression of endogenous miR-21-targets Pdcd4, PTEN and Bcl-2. siRNA knockdown of ER alpha blocked the E (2)-induced increase in Pdcd4, PTEN and Bcl-2. |
2(0,0,0,2) | 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 |
| 17097066 | Lee TJ, Lee JT, Park JW, Kwon TK: Acquired TRAIL resistance in human breast cancer cells are caused by the sustained cFLIP (L) and XIAP protein levels and ERK activation. Biochem Biophys Res Commun. 2006 Dec 29;351(4):1024-30. Epub 2006 Nov 7. The selected TRAIL-resistant cells were cross-resistant to TNF-alpha/cycloheximide but remained sensitive to DNA-damage drugs such as oxaliplatin and etoposide. |
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. |
3(0,0,0,3) | Details |
| 15844877 | Jaganathan J, Petit JH, Lazio BE, Singh SK, Chin LS: Tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in established and primary glioma cell lines. Neurosurg Focus. 2002 Sep 15;13(3):ecp1. Finally, to study the direct effects of DR5 on glioma cells, the authors conducted transient and stable transfections of the full-length DR5 transcript into glioma cells with and without preestablished overexpression of the antiapoptotic gene bcl-2. The A172 cells, by contrast, were susceptible only with cycloheximide, whereas U373MG cells were not susceptible to TRAIL. |
3(0,0,0,3) | 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 |
| 16136269 | Danforth DN, Zhu Y: Conversion of Fas-resistant to Fas-sensitive MCF-7 breast cancer cells by the synergistic interaction of interferon-gamma and Breast Cancer Res Treat. 2005 Nov;94(1):81-91. FasR-induced cells were resistant to stimulation of apoptosis by anti-FasR antibody, however treatment with cycloheximide rendered these cells sensitive to antibody-induced apoptosis, suggesting endogenous blockade to signaling. |
0(0,0,0,0) | Details |
| 18719002 | Pritchard DM, Berry D, Przemeck SM, Campbell F, Edwards SW, Varro A: Gastrin increases mcl-1 expression in type I gastric carcinoid tumors and a gastric epithelial cell line that expresses the CCK-2 receptor. Am J Physiol Gastrointest Liver Physiol. 2008 Oct;295(4):G798-805. Epub 2008 Aug 21. We hypothesized that the antiapoptotic effects of gastrin may be implicated and have therefore investigated the role of antiapoptotic members of the bcl-2 family of proteins. Gastrin-induced mcl-1 expression was inhibited by the transcription inhibitor actinomycin D and by the protein synthesis inhibitor cycloheximide. |
2(0,0,0,2) | Details |
| 19183465 | Gentilini A, Lottini B, Brogi M, Caligiuri A, Cosmi L, Marra F, Pinzani M: Evaluation of intracellular signalling pathways in response to insulin-like growth factor I in apoptotic-resistant activated human hepatic stellate cells. Fibrogenesis Tissue Repair. 2009 Jan 30;2(1):1. In particular, previous studies have demonstrated an increased expression of the anti-apoptotic protein Bcl-2 and a decreased expression of the pro-apoptotic protein Bax during the transition of the hepatic stellate cell phenotype from quiescent to myofibroblast-like cells. |
2(0,0,0,2) | Details |
| 16094403 | Kucharczak JF, Simmons MJ, Duckett CS, Gelinas C: Constitutive proteasome-mediated turnover of Bfl-1/A1 and its processing in response to TNF receptor activation in FL5.12 pro-B cells convert it into a prodeath factor. Cell Death Differ. 2005 Sep;12(9):1225-39. Bfl-1/A1 is generally recognized as a Bcl-2-related inhibitor of apoptosis. Its anti- versus proapoptotic effect is regulated by two proteolytic events: (1) its constitutive proteasome-mediated turnover and (2) its TNF/cycloheximide (CHX)-induced cleavage by mu-calpain, or a calpain-like activity, coincident with acquisition of a proapoptotic phenotype. |
2(0,0,0,2) | Details |
| 17045260 | Orozco C, Garcia-de-Diego AM, Arias E, Hernandez-Guijo JM, Garcia AG, Villarroya M, Lopez MG: Depolarization preconditioning produces cytoprotection against veratridine-induced chromaffin cell death. Eur J Pharmacol. 2006 Dec 28;553(1-3):28-38. Epub 2006 Sep 12. Preconditioning with K (+) or TEA increased by 2.5-fold the expression of brain-derived neurotrophic factor and by nearly 2-fold the expression of the antiapoptotic protein Bcl-2. |
2(0,0,0,2) | Details |
| 16675490 | Chang AY, Chan JY, Chou JL, Li FC, Dai KY, Chan SH: Heat shock protein 60 in rostral ventrolateral medulla reduces cardiovascular fatality during endotoxaemia in the rat. J Physiol. 2006 Jul 15;574(Pt 2):547-64. Epub 2006 May 4. Pretreatment with a microinjection of actinomycin D or cycloheximide into bilateral RVLM significantly blunted this HSP60 increase, whereas real-time PCR showed progressive augmentation of hsp60 mRNA. Immunoprecipitation coupled with immunoblot analysis further revealed a progressive increase in the complex formed between HSP60 and mitochondrial or cytosolic Bax or mitochondrial Bcl-2 during endotoxaemia, alongside a dissociation of the cytosolic HSP60-Bcl-2 complex. |
2(0,0,0,2) | Details |
| 15977640 | Nowoslawski L, Klocke BJ, Roth KA: Molecular regulation of acute -induced neuron apoptosis. J Neuropathol Exp Neurol. 2005 Jun;64(6):490-7. We have previously demonstrated that -induced neuron apoptosis is critically dependent on expression of Bax, a proapoptotic member of the Bcl-2 family. |
2(0,0,0,2) | Details |
| 18056701 | Fei Q, McCormack AL, Di Monte DA, Ethell DW: Paraquat neurotoxicity is mediated by a Bak-dependent mechanism. . J Biol Chem. 2008 Feb 8;283(6):3357-64. Epub 2007 Dec 4. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. |
2(0,0,0,2) | Details |
| 16546987 | Tang R, Faussat AM, Majdak P, Marzac C, Dubrulle S, Marjanovic Z, Legrand O, Marie JP: Semisynthetic homoharringtonine induces apoptosis via inhibition of protein synthesis and triggers rapid myeloid cell leukemia-1 down-regulation in myeloid leukemia cells. Mol Cancer Ther. 2006 Mar;5(3):723-31. To unveil the relationship between ssHHT and the mitochondrial disruption, we have shown that ssHHT decreased myeloid cell leukemia-1 (Mcl-1) expression and induced Bcl-2 cleavage in HL60 and HL60/MRP cell lines. The Mcl-1 turnover was only induced by ssHHT and cycloheximide, but not by daunorubicin and cytosine arabinoside, and could be restored by proteasome inhibitors. |
2(0,0,0,2) | 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. |
2(0,0,0,2) | 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. While the ectopic expression of the anti-apoptoticprotein Bcl-2 has been shown to significantly increaseboth cell viability and antibody production in batchculture, some cell lines are refractory to thesemanipulations. This murine hybridomaexpresses low levels of Bcl-xL and is highly sensitiveto apoptosis induction by cycloheximide (CHX) and byamino acid depletion. |
2(0,0,0,2) | Details |
| 16251184 | Almeida M, Han L, Bellido T, Manolagas SC, Kousteni S: Wnt proteins prevent apoptosis of both uncommitted osteoblast progenitors and differentiated osteoblasts by beta-catenin-dependent and -independent signaling cascades involving Src/ERK and phosphatidylinositol 3-kinase/AKT. J Biol Chem. 2005 Dec 16;280(50):41342-51. Epub 2005 Oct 25. The anti-apoptotic effect of Wnt3a was abrogated by inhibitors of canonical Wnt signaling, as well as by inhibitors of MEK, Src, phosphatidylinositol 3-kinase (PI3K), or Akt kinases, or by the addition of cycloheximide to the culture medium. Wnt3a increased the expression of the anti-apoptotic protein Bcl-2 in an ERK-dependent manner. |
1(0,0,0,1) | Details |
| 16152591 | Akahane M, Akahane T, Matheny SL, Shah A, Okajima E, Thorgeirsson UP: Vascular endothelial growth factor-D is a survival factor for human breast carcinoma cells. Int J Cancer. 2006 Feb 15;118(4):841-9. The VEGF-D-expressing MCF-7 and MDA-MB-231 lines displayed resistance to apoptosis induced by hypoxia, staurosporin and cycloheximide. Increased Bcl-2 expression, decreased homogenous caspase activities and inhibition of poly (ADP- polymerase cleavage were associated with inhibition of apoptosis in VEGF-D-expressing clones. |
1(0,0,0,1) | Details |
| 18078929 | Brumatti G, Yon M, Castro FA, Bueno-da-Silva AE, Jacysyn JF, Brunner T, Amarante-Mendes GP: Conversion of CD95 (Fas) Type II into Type I signaling by sub-lethal doses of cycloheximide. Exp Cell Res. 2008 Feb 1;314(3):554-63. Epub 2007 Nov 17. Moreover, Bcl-2-positive Type II cells become strongly sensitive to CD95-mediated apoptosis by the addition of CHX to the cell culture. |
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 |
| 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. The ectopic expression of several members of the Bcl-2 family of anti-apoptotic proteins is a promising strategy to improve the viability of hybridoma cells in culture. 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. |
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 |
| 20028813 | Massari P, Gunawardana J, Liu X, Wetzler LM: Meningococcal porin PorB prevents cellular apoptosis in a toll-like receptor 2- and NF-kappaB-independent manner. Infect Immun. 2010 Mar;78(3):994-1003. Epub 2009 Dec 22. Interestingly, PorB does not prevent extrinsic apoptosis induced by tumor necrosis factor alpha plus cycloheximide, suggesting a unique mitochondrial pathway specificity. Several intracellular factors regulated by NF-kappaB, including members of the Bcl-2 family and of the inhibitor of apoptosis (IAP) family, play major roles in controlling apoptosis, and some of them are thought to contribute to the antiapoptotic effect of the gonococcal porin, PIB. |
1(0,0,0,1) | Details |
| 18331646 | Feng P, Li T, Guan Z, Franklin RB, Costello LC: The involvement of Bax in zinc-induced mitochondrial apoptogenesis in malignant prostate cells. Mol Cancer. 2008 Mar 10;7:25. The mitochondrial Bax/Bcl-2 ratio is increased by zinc treatment. |
1(0,0,0,1) | Details |
| 16034370 | Ma D, Hossain M, Pettet GK, Luo Y, Lim T, Akimov S, Sanders RD, Franks NP, Maze M: Xenon preconditioning reduces brain damage from neonatal asphyxia in rats. J Cereb Blood Flow Metab. 2006 Feb;26(2):199-208. In a neuronal-glial cell coculture, preexposure to xenon for 2 h caused a concentration-dependent reduction of lactate dehydrogenase release from cells deprived of and 24 h later; xenon's preconditioning effect was abolished by cycloheximide, a protein synthesis inhibitor. Also, the prosurvival proteins Bcl-2 and brain-derived neurotrophic factor were upregulated by xenon treatment. |
1(0,0,0,1) | Details |
| 16626937 | Catts VS, Catts SV, McGrath JJ, Feron F, McLean D, Coulson EJ, Lutze-Mann LH: Apoptosis and schizophrenia: a pilot study based on dermal fibroblast cell lines. Schizophr Res. 2006 May;84(1):20-8. Epub 2006 Apr 19. Susceptibility to apoptosis was measured at the level of degradation product (proportion of cells in the sub-G0 cell cycle fraction in which apoptotic bodies accumulate), pro-apoptotic effector (activated caspase-3), and molecular regulators (P53, Bax and Bcl-2). Cell lines were studied under both basal culture and cycloheximide (an apoptotic inducer) exposure conditions. |
1(0,0,0,1) | Details |
| 18069034 | Ying S, Christian JG, Paschen SA, Hacker G: Chlamydia trachomatis can protect host cells against apoptosis in the absence of cellular Inhibitor of Apoptosis Proteins and Mcl-1. Microbes Infect. 2008 Jan;10(1):97-101. Epub 2007 Oct 18. Hypotheses have been proposed to explain this molecularly, including the up-regulation of host anti-apoptotic proteins such as cellular Inhibitor of Apoptosis Protein (IAP) 2 and the Bcl-2 protein Mcl-1. Infection with Chlamydia trachomatis protected all cells equally well against apoptosis, which was induced either with tumour necrosis factor/cycloheximide (IAP-knock-out cells) or staurosporine (Mcl-1-knock-out). |
1(0,0,0,1) | Details |
| 16888780 | Wieckowski E, Atarashi Y, Stanson J, Sato TA, Whiteside TL: FAP-1-mediated activation of NF-kappaB induces resistance of head and neck cancer to Fas-induced apoptosis. J Cell Biochem. 2007 Jan 1;100(1):16-28. In the presence of cycloheximide, the selected SCCHN sublines become susceptible to CH-11 Ab, and showed cleavage of caspase-8, suggesting that apoptosis resistance was mediated by an inhibitory protein (s) acting upstream of caspase-8. A high phosphorylation level of IkappaB kappa, NFkappaB activation and upregulation of Bcl-2 expression were observed in the FAP-1+ sublines. |
1(0,0,0,1) | 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 |
| 16479541 | Nencioni A, Garuti A, Schwarzenberg K, Cirmena G, Dal Bello G, Rocco I, Barbieri E, Brossart P, Patrone F, Ballestrero A: Proteasome inhibitor-induced apoptosis in human monocyte-derived dendritic cells. Eur J Immunol. 2006 Mar;36(3):681-9. Up-regulation and intracellular redistribution of Bcl-2-associated X protein (Bax), a pro-apoptotic Bcl-2 family protein, were observed in DC treated with these compounds and represent a suitable mechanism leading to activation of the intrinsic apoptotic pathway. Finally, active protein synthesis was found to represent an upstream prerequisite for DC apoptosis induced by proteasome inhibitors, since the translation inhibitor cycloheximide blocked all of the steps of the observed apoptotic response. |
1(0,0,0,1) | Details |
| 17535899 | Fu NY, Sukumaran SK, Yu VC: Inhibition of ubiquitin-mediated degradation of MOAP-1 by apoptotic stimuli promotes Bax function in mitochondria. Proc Natl Acad Sci U S A. 2007 Jun 12;104(24):10051-6. Epub 2007 May 29. The multidomain proapoptotic protein Bax of the Bcl-2 family is a central regulator for controlling the release of apoptogenic factors from mitochondria. Mitochondria depleted of short-lived proteins by cycloheximide (CHX) become resistant to Bax-mediated cytochrome c release. |
1(0,0,0,1) | 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. However, the molecular mechanism through which PUMA regulates apoptosis, especially how PUMA activates Bcl-2-associated X protein (Bax) in response to UV irradiation is still controversial. In addition, pifithrin-alpha (a p53 inhibitor) and cycloheximide (a protein synthesis inhibitor) could inhibit PUMA-mediated Bax translocation and cell apoptosis. |
1(0,0,0,1) | Details |
| 19952118 | Ballot C, Kluza J, Martoriati A, Nyman U, Formstecher P, Joseph B, Bailly C, Marchetti P: Essential role of mitochondria in apoptosis of cancer cells induced by the marine alkaloid Lamellarin D. Mol Cancer Ther. 2009 Dec;8(12):3307-17. Epub . However, lamellarin D killed efficiently mutated p53 or p53 null cancer cells, and sensitivity to lamellarin D was abrogated neither by cycloheximide nor in enucleated cells. The drug induced conformational activation of Bax and decreased the expression levels of antiapoptotic proteins Bcl-2 and cIAP2 in association with activation of caspase-9 and caspase-3. |
1(0,0,0,1) | Details |
| 17311906 | Yang C, Kaushal V, Shah SV, Kaushal GP: Mcl-1 is downregulated in cisplatin-induced apoptosis, and proteasome inhibitors restore Mcl-1 and promote survival in renal tubular epithelial cells. Am J Physiol Renal Physiol. 2007 Jun;292(6):F1710-7. Epub 2007 Feb 20. Mcl-1 is an antiapoptotic member of the Bcl-2 family that plays an important role in cell survival. Treatment of cells with cycloheximide, a protein synthesis inhibitor, revealed rapid turnover of Mcl-1. |
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. However, the roles of prosurvival Bcl-2 family proteins in TRAIL apoptosis remain elusive. In sharp contrast to cycloheximide-induced Mcl-1 dilapidation, TRAIL did not activate proteasomal degradation of Mcl-1 in Jurkat cells. |
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| 16876795 | Kato T, Kutsuna H, Oshitani N, Kitagawa S: delays neutrophil apoptosis via stabilization of Mcl-1. . FEBS Lett. 2006 Aug 21;580(19):4582-6. Epub 2006 Jul 21. Spontaneous neutrophil apoptosis and Mcl-1 degradation were prevented by (cAMP) agonists (dibutyryl cAMP and (1)), and the effects of cAMP agonists on neutrophils were highly resistant to cycloheximide, a protein synthesis inhibitor, although slight increase in Mcl-1 mRNA expression was induced by cAMP agonists. |
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