| Name | mcl 1 |
|---|---|
| Synonyms | Bcl 2 related protein EAT/mcl1; EAT; Induced myeloid leukemia cell differentiation protein Mcl 1; MCL 1; MCL1; MCL1L; MCL1S; Myeloid cell leukemia 1… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. |
83(1,1,1,3) | Details |
| 18647593 | Ozaki Y, Kato T, Kitagawa M, Fujita H, Kitagawa S: Calpain inhibition delays neutrophil apoptosis via cyclic AMP-independent activation of protein kinase A and protein kinase A-mediated stabilization of Mcl-1 and X-linked inhibitor of apoptosis (XIAP). Arch Biochem Biophys. 2008 Sep 15;477(2):227-31. Epub 2008 Jul 11. Calpain inhibitors (PD150606 and N-acetyl---Nle-CHO) prevented spontaneous neutrophil apoptosis and degradation of Mcl-1 and XIAP, and the effects of calpain inhibitors on neutrophils were resistant to cycloheximide. |
35(0,1,1,5) | Details |
| 16109713 | Rahmani M, Davis EM, Bauer C, Dent P, Grant S: Apoptosis induced by the kinase inhibitor BAY 43-9006 in human leukemia cells involves down-regulation of Mcl-1 through inhibition of translation. J Biol Chem. 2005 Oct 21;280(42):35217-27. Epub 2005 Aug 18. Inhibition of protein synthesis by cycloheximide or proteasome function with MG132 and pulse-chase studies with [35S] demonstrated that BAY 43-9006 did not diminish Mcl-1 protein stability, nor did it enhance Mcl-1 ubiquitination, but instead markedly attenuated Mcl-1 translation in association with the rapid and potent dephosphorylation of the eIF4E translation initiation factor. |
4(0,0,0,4) | 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. |
4(0,0,0,4) | Details |
| 18678651 | Chu C, Shatkin AJ: Apoptosis and autophagy induction in mammalian cells by small interfering RNA knockdown of mRNA capping enzymes. Mol Cell Biol. 2008 Oct;28(19):5829-36. Epub 2008 Aug 4. In addition, levels of the BH3 family member Bim increased, while Mcl-1 and Bik levels remained unchanged during apoptosis. Both Bim and Mcl-1 levels decreased in cycloheximide-induced apoptosis while Bik levels were unchanged, suggesting that apoptosis in siRNA-treated cells is not a direct consequence of loss of mRNA translation. siRNA-treated BAK (-/-) BAX (-/-) double-knockout mouse embryonic fibroblasts failed to activate capase-3 or increase TUNEL staining but instead exhibited autophagy, as demonstrated by proteolytic processing of microtubule-associated protein 1 light chain 3 (LC3) and translocation of transfected green fluorescent protein-LC3 from the nucleus to punctate cytoplasmic structures. |
1(0,0,0,1) | Details |
| 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. Overexpression of Mcl-1 blocked apoptosis induced by cycloheximide, whereas RNA interference knockdown of Mcl-1 induced apoptosis. |
166(2,2,2,6) | 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. Treatment of cells with cycloheximide, a protein synthesis inhibitor, revealed rapid turnover of Mcl-1. |
119(1,2,2,9) | 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. Gastrin-induced mcl-1 expression was inhibited by the transcription inhibitor actinomycin D and by the protein synthesis inhibitor cycloheximide. |
38(0,1,1,8) | 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. 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). |
9(0,0,1,4) | 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. |
4(0,0,0,4) | 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. 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. |
4(0,0,0,4) | Details |
| 16029896 | Oguma K, Sano J, Kano R, Watari T, Moritomo T, Hasegawa A: In vitro effect of recombinant human granulocyte colony-stimulating factor on canine neutrophil apoptosis. Vet Immunol Immunopathol. 2005 Dec 15;108(3-4):307-14. Epub 2005 Jul 18. The addition of cycloheximide abolished this suppression by rhG-CSF. Moreover, canine PMNs, which were stimulated by rhG-CSF, expressed high levels of anti-apoptotic mcl-1 gene mRNA, as quantified by real-time polymerase chain reaction method. |
2(0,0,0,2) | Details |
| 19457567 | Jiang JX, Mikami K, Venugopal S, Li Y, Torok NJ: Apoptotic body engulfment by hepatic stellate cells promotes their survival by the JAK/STAT and Akt/NF-kappaB-dependent pathways. J Hepatol. 2009 Jul;51(1):139-48. Epub 2009 May 3. The JAK/STAT- and PI3K/Akt-dependent pathways, NF-kappaB activation and expression of the anti-apoptotic proteins Mcl-1 and A1 were evaluated. RESULTS: Phagocytosing HSC were resistant to FasL/cycloheximide or TRAIL-induced apoptosis. |
2(0,0,0,2) | 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. We attribute this effect to a reduction in levels of pro-oncogenic or pro-survival proteins having short half-lives, like Mcl-1, cyclin D1 or c-Myc. |
1(0,0,0,1) | 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. TNF-alpha-induced JNK phosphorylation was sustained in the presence of cycloheximide, which was accompanied by accelerated neutrophil apoptosis. |
0(0,0,0,0) | Details |