Name | tumor necrosis factor alpha |
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Synonyms | Cachectin; DIF; TNF; TNF alpha; TNF a; TNFA; TNFSF 2; TNFSF2… |
Name | cycloheximide |
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CAS |
PubMed | Abstract | RScore(About this table) | |
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17416199 | Choi EM: inhibits tumor necrosis factor-alpha-induced production of interleukin-6 and in osteoblastic MC3T3-E1 cells. Pharmazie. 2007 Mar;62(3):216-20. The effect of in increasing ALP activity and collagen content was completely prevented by the presence of 10 (-6) M cycloheximide and 10-6 M tamoxifen, suggesting that apigenin's effect results from a newly synthesized protein component and might be partly involved in action. |
increases osteoblastic differentiation and 1(0,0,0,1) | Details |
15629516 | Okuyama H, Nakamura H, Shimahara Y, Uyama N, Kwon YW, Kawada N, Yamaoka Y, Yodoi J: Overexpression of thioredoxin prevents thioacetamide-induced hepatic fibrosis in mice. J Hepatol. 2005 Jan;42(1):117-23. Overexpression of thioredoxin inhibited tumor necrosis factor-alpha-induced apoptosis of HepG2 cells. |
1(0,0,0,1) | Details |
16479515 | Green J, Khabar KS, Koo BC, Williams BR, Polyak SJ: Stability of CXCL-8 and related AU-rich mRNAs in the context of hepatitis C virus replication in vitro. J Infect Dis. 2006 Mar 15;193(6):802-11. Epub 2006 Feb 13. METHODS: The half-life of CXCL-8 mRNA was measured by use of real-time reverse-transcription polymerase chain reaction following tumor necrosis factor (TNF)- alpha induction in the presence and absence of inhibitors of transcription and translation. CXCL-8 mRNA was superinduced by TNF- alpha in the presence of the protein-synthesis inhibitor cycloheximide. |
1(0,0,0,1) | Details |
15639338 | Hofmanova J, Vaculova A, Kozubik A: Polyunsaturated fatty acids sensitize human colon adenocarcinoma HT-29 cells to death receptor-mediated apoptosis. Cancer Lett. 2005 Jan 31;218(1):33-41. The proliferative and apoptotic response to TNF-alpha and anti-Fas antibody (CH-11) in human colon adenocarcinoma HT-29 cells was modulated by pretreatment with arachidonic (AA, 20:4, n-6) or docosahexaenoic 22:6, n-3) fatty acids, which alone increased reactive species production and lipid peroxidation, and decreased the S-phase of the cell cycle. The higher amount of floating cells, subG0/G1 population and apoptotic cells detected in pre-treated cells was potentiated by cycloheximide. |
1(0,0,0,1) | Details |
16514055 | Gu BJ, Wiley JS: Rapid ATP-induced release of matrix metalloproteinase 9 is mediated by the P2X7 receptor. Blood. 2006 Jun 15;107(12):4946-53. Epub 2006 Mar 2. ATP-induced MMP-9 release was inhibited by the P2X (7) receptor antagonists periodate oxidized ATP and KN-62, or by chelators, as well as by a loss-of-function polymorphism in the P2X (7) receptor, but not by brefeldin A, monensin, or cycloheximide, or by anti-tumor necrosis factor-alpha (TNF-alpha) or anti-interleukin-1beta (IL-1beta) monoclonal antibodies. |
0(0,0,0,0) | Details |
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. |
31(0,1,1,1) | Details |
15856013 | Yuan H, Fu F, Zhuo J, Wang W, Nishitani J, An DS, Chen IS, Liu X: Human papillomavirus type 16 E6 and E7 oncoproteins upregulate c-IAP2 gene expression and confer resistance to apoptosis. Oncogene. 2005 Jul 28;24(32):5069-78. Overexpression of c-IAP2 in normal human oral keratinocyte conferred resistance to tumor necrosis factor-alpha (TNF-alpha)/cycloheximide (CHX)-induced apoptosis, suggesting the increased c-IAP2 expression in HOK16E6E7 may protect the cells from TNF-alpha-mediated cell death. |
31(0,1,1,1) | Details |
18442799 | Ogura H, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: ERK and p38 MAP kinase are involved in downregulation of cell surface TNF receptor 1 induced by acetoxycycloheximide. Int Immunopharmacol. 2008 Jun;8(6):922-6. Epub 2008 Mar 18. Tumor necrosis factor (TNF)-alpha activates the nuclear factor kappaB (NF-kappaB) signaling pathway. The protein synthesis inhibitor cycloheximide (CHX) and its structural derivative acetoxycycloheximide (Ac-CHX) have been recently shown to block the TNF-alpha-induced activation of NF-kappaB via ectodomain shedding of TNF receptor 1 (TNF-R1) in human lung carcinoma A549 cells. |
1(0,0,0,1) | Details |
17453339 | Guseva NV, Rokhlin OW, Taghiyev AF, Cohen MB: Unique resistance of breast carcinoma cell line T47D to TRAIL but not anti-Fas is linked to p43cFLIP (L). Breast Cancer Res Treat. 2008 Feb;107(3):349-57. Epub 2007 Apr 24. The majority of breast cancer cell lines are resistant to tumor necrosis factor -related apoptosis inducing ligand (TRAIL) induced apoptosis. |
1(0,0,0,1) | Details |
16799629 | Obeid D, Nguyen J, Lesavre P, Bauvois B: Differential regulation of tumor necrosis factor-alpha-converting enzyme and angiotensin-converting enzyme by type I and II interferons in human normal and leukemic myeloid cells. Oncogene. 2007 Jan 4;26(1):102-10. Epub 2006 Jun 26. The transmembrane metalloproteases angiotensin-converting enzyme (ACE) and tumor necrosis factor-alpha (TNF-alpha)-converting enzyme (TACE/ADAM-17) have been associated with inflammation, cancer progression and angiogenesis. |
1(0,0,0,1) | Details |
17211541 | Johns P, Pereira SL, Leonard AE, Mukerji P, Shalwitz RA, Dowlati L, Phillips RR, Bergana MS, Holton JD, Das T: Cytoprotective agent in Lactobacillus bulgaricus extracts. Curr Microbiol. 2007 Feb;54(2):131-5. Epub 2007 Jan 5. levels as low as 5 mg/L exhibited a measurable inhibition of tumor necrosis factor alpha (TNF-alpha) mediated cytotoxicity in an in vitro cell assay, whereas the content of the L. bulgaricus extracts often exceeded 5 mg/g dry weight. |
1(0,0,0,1) | Details |
17069807 | Birbes H, Zeiller C, Komati H, Nemoz G, Lagarde M, Prigent AF: Phospholipase D protects ECV304 cells against TNFalpha-induced apoptosis. FEBS Lett. 2006 Nov 13;580(26):6224-32. Epub 2006 Oct 19. Using ECV304 cells, which can be made TNFalpha-sensitive by cycloheximide (CHX) co-treatment, we evaluated the potential roles of and phospholipase D (PLD) in TNFalpha-induced apoptosis. |
11(0,0,1,6) | Details |
19289468 | Kurada BR, Li LC, Mulherkar N, Subramanian M, Prasad KV, Prabhakar BS: MADD, a splice variant of IG20, is indispensable for MAPK activation and protection against apoptosis upon tumor necrosis factor-alpha treatment. J Biol Chem. 2009 May 15;284(20):13533-41. Epub 2009 Mar 16. Abrogation of MADD expression rendered cells highly susceptible to TNFalpha-induced apoptosis in the absence of cycloheximide. |
11(0,0,1,6) | Details |
16546965 | Lane D, Cote M, Grondin R, Couture MC, Piche A: Acquired resistance to TRAIL-induced apoptosis in human ovarian cancer cells is conferred by increased turnover of mature caspase-3. Mol Cancer Ther. 2006 Mar;5(3):509-21. Little is known on how cancer cells can acquire resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Pretreatment with cycloheximide showed that active caspase-3 fragments have a high turnover rate in OVCAR3 R350 cells. |
1(0,0,0,1) | Details |
16985255 | Floyd ZE, Segura BM, He F, Stephens JM: Degradation of STAT5 proteins in 3T3-L1 adipocytes is induced by TNF-{alpha} and cycloheximide in a manner independent of STAT5A activation. Am J Physiol Endocrinol Metab. 2007 Feb;292(2):E461-8. Epub 2006 Sep 19. Tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine that has been implicated as a causative factor in obesity-linked insulin resistance. |
1(0,0,0,1) | Details |
16822952 | Basuroy S, Bhattacharya S, Tcheranova D, Qu Y, Regan RF, Leffler CW, Parfenova H: HO-2 provides endogenous protection against oxidative stress and apoptosis caused by TNF-alpha in cerebral vascular endothelial cells. Am J Physiol Cell Physiol. 2006 Nov;291(5):C897-908. Epub 2006 Jul 5. Tumor necrosis factor-alpha (TNF-alpha) causes oxidative stress and apoptosis in a variety of cell types. In CMVEC from mice and newborn pigs, 15 ng/ml TNF-alpha alone, or with 10 microg/ml cycloheximide (CHX) caused apoptosis detected by nuclear translocation of p65 NF-kappaB, caspase-3 activation, DNA fragmentation, cell-cell contact destabilization, and cell detachment. |
1(0,0,0,1) | Details |
17492827 | Chung MJ, Liu T, Ullenbruch M, Phan SH: Antiapoptotic effect of found in inflammatory zone (FIZZ) 1 on mouse lung fibroblasts. J Pathol. 2007 Jun;212(2):180-7. Cells were treated with FIZZ1 for 24 h and then apoptosis was induced by TNFalpha in the presence of cycloheximide (CHX). |
1(0,0,0,1) | Details |
18445680 | Solinet S, Vitale ML: Isoform B of myosin II heavy chain mediates actomyosin contractility during TNFalpha-induced apoptosis. J Cell Sci. 2008 May 15;121(Pt 10):1681-92. Epub 2008 Apr 29. Cells that are treated long-term with TNFalpha or short-term with TGFalpha together with cycloheximide (CHX) undergo apoptosis. |
10(0,0,1,5) | Details |
16508982 | D'Osualdo A, Ferlito F, Prigione I, Obici L, Meini A, Zulian F, Pontillo A, Corona F, Barcellona R, Di Duca M, Santamaria G, Traverso F, Picco P, Baldi M, Plebani A, Ravazzolo R, Ceccherini I, Martini A, Gattorno M: Neutrophils from patients with TNFRSF1A mutations display resistance to tumor necrosis factor-induced apoptosis: pathogenetic and clinical implications. Arthritis Rheum. 2006 Mar;54(3):998-1008. Neutrophils were isolated from heparinized blood by dextran sedimentation and incubated with and without cycloheximide (CHX) and TNFalpha. |
8(0,0,1,3) | Details |
16910777 | Dasgupta J, Subbaram S, Connor KM, Rodriguez AM, Tirosh O, Beckman JS, Jourd'Heuil D, Melendez JA: Manganese superoxide dismutase protects from TNF-alpha-induced apoptosis by increasing the steady-state production of H2O2. Antioxid Redox Signal. 2006 Jul-Aug;8(7-8):1295-305. Here we demonstrate that the antiapoptotic effects of SOD2 are attributed to its ability to generate H (2) O (2) and that its efficient removal resensitizes cells to tumor necrosis factor (TNF)-alpha-induced apoptosis. |
1(0,0,0,1) | Details |
16036110 | Zhang L, Zhu H, Teraishi F, Davis JJ, Guo W, Fan Z, Fang B: Accelerated degradation of caspase-8 protein correlates with TRAIL resistance in a DLD1 human colon cancer cell line. Neoplasia. 2005 Jun;7(6):594-602. The tumor-selective cytotoxic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) makes TRAIL an attractive candidate as an anticancer agent. |
1(0,0,0,1) | Details |
15832948 | Concannon CG, FitzGerald U, Holmberg CI, Szegezdi E, Sistonen L, Samali A: CD95-mediated alteration in Hsp70 levels is dependent on protein stabilization. Cell Stress Chaperones. 2005 Spring;10(1):59-65. Inhibition of translation and de novo protein synthesis by cycloheximide resulted in Hsp70 protein levels diminishing over time in control cells, whereas its level remained constant during CD95 signaling. |
0(0,0,0,0) | Details |
17529908 | Xing L, Remick DG: Mechanisms of oxidant regulation of monocyte chemotactic protein 1 production in human whole blood and isolated mononuclear cells. Shock. 2007 Aug;28(2):178-85. Cycloheximide treatment did not abolish the DMSO inhibition of MCP-1 mRNA, demonstrating that de novo protein synthesis is not required. |
0(0,0,0,0) | Details |
16003319 | Mori T, Doi R, Toyoda E, Koizumi M, Ito D, Kami K, Kida A, Masui T, Kawaguchi Y, Fujimoto K: Regulation of the resistance to TRAIL-induced apoptosis as a new strategy for pancreatic cancer. Surgery. 2005 Jul;138(1):71-7. In the TRAIL-resistant pancreatic cancer cells, effects of cycloheximide, a protein synthesis inhibitor, on death signal-transducing proteins were tested. |
0(0,0,0,0) | Details |
19709659 | Cancel LM, Tarbell JM: The role of apoptosis in LDL transport through cultured endothelial cell monolayers. Atherosclerosis. 2010 Feb;208(2):335-41. Epub 2009 Aug 7. To explore the role of apoptosis in the leaky junction pathway, TNFalpha and cycloheximide (TNFalpha/CHX) were used to induce an elevated rate of apoptosis in cultured bovine aortic endothelial cell (BAEC) monolayers and the convective fluxes of LDL and water were measured. |
8(0,0,1,3) | Details |
16325265 | Sylte MJ, Kuckleburg CJ, Leite FP, Inzana TJ, Czuprynski CJ: Tumor necrosis factor-alpha enhances Haemophilus somnus lipooligosaccharide-induced apoptosis of bovine endothelial cells. Vet Immunol Immunopathol. 2006 Apr 15;110(3-4):303-9. Epub 2005 Dec 1. However, blocking de novo protein synthesis by addition of cycloheximide significantly enhanced apoptosis of bovine endothelial cells by TNF-alpha, LOS or TNF-alpha and LOS in combination. |
1(0,0,0,1) | Details |
17900782 | Kumagai K, Kiyosawa N, Ito K, Yamoto T, Teranishi M, Nakayama H, Manabe S: Influence of Kupffer cell inactivation on cycloheximide-induced hepatic injury. Toxicology. 2007 Nov 30;241(3):106-18. Epub 2007 Aug 25. Thus, Kupffer cell inactivation by the GdCl (3) treatment leads to a loss of the capacity to produce IL-10, supposedly resulting in the enhancement of pro-inflammatory cytokine activities such as tumor necrosis factor (TNF) signaling. |
1(0,0,0,1) | Details |
17659437 | Reidy MR, Ellis J, Schmitz EA, Kraus DM, Bulla GA: Apoptosis of dedifferentiated hepatoma cells is independent of NF-kappaB activation in response to LPS. Biosci Rep. 2007 Oct;27(4-5):235-46. Dedifferentiated hepatoma cells, in contrast to most other cell types including hepatoma cells, undergo apoptosis when treated with lipopolysaccharide (LPS) plus the protein synthesis inhibitor cycloheximide (CHx). These results suggest that unlike TNFalpha induction, the cell survival pathway activated in response to LPS is independent of NF-kappaB translocation in the dedifferentiated cells. |
1(0,0,0,1) | Details |
17368935 | Choi EM: Modulatory effects of function and inflammatory mediators in osteoblastic MC3T3-E1 cells. Cell Biol Int. 2007 Sep;31(9):870-7. Epub 2007 Feb 11. The effect of in increasing collagen content and ALP activity was completely prevented by the presence of 10 (-6) M cycloheximide and 10 (-6) M tamoxifen, suggesting that luteolin's effect results from a newly synthesized protein component and might be partly involved in action. We then examined the effect of on the 3-morpholinosydnonimine (SIN-1)-induced production of oxidative stress markers (NO) and prostaglan E (2) (PGE (2))] and cytokines [tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6)] in osteoblasts. |
on osteoblastic 1(0,0,0,1) | Details |
16595663 | Castellano R, Vire B, Pion M, Quivy V, Olive D, Hirsch I, Van Lint C, Collette Y: Active transcription of the human FASL/CD95L/TNFSF6 promoter region in T lymphocytes involves chromatin remodeling: role of DNA methylation and protein acetylation suggest distinct mechanisms of transcriptional repression. J Biol Chem. 2006 May 26;281(21):14719-28. Epub 2006 Apr 4. Fas ligand (FasL/CD95L/TNFSF6), a member of the tumor necrosis factor family, initiates apoptosis in lymphoid and nonlymphoid tissues by binding to its receptor Fas (CD95/TNFRSF6). HSS1 chromatin remodeling preceded detectable TNFSF6 mRNA accumulation and was blocked by cycloheximide that also prevented TNFSF6 transcription. |
1(0,0,0,1) | 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. The pathway of interferon-gamma (IFN-gamma)-induced suppression in tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-mediated apoptosis of fibroblast-like synovial cells (FLS) was investigated. rTRAIL triggered FLS apoptosis in a type II cell death manner, whereas IFN-gamma pretreatment significantly inhibited TRAIL-mediated apoptosis. 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. |
1(0,0,0,1) | Details |
17200614 | Pandey M, Bajaj GD, Rath PC: Induction of the interferon-inducible RNA-degrading enzyme, RNase L, by stress-inducing agents in the human cervical carcinoma cells. RNA Biol. 2004 May;1(1):21-7. Epub 2004 May 5. We report that RNase L is induced by stress-inducing agents such as double-stranded RNA [poly (I:C)], chemotherapeutic drugs, peroxide (H (2) O (2)), calcium chloride (CaCl (2)) and tumor necrosis factor-alpha (TNF) in the human cervical carcinoma (HeLa) cells. We checked the stress-inducible transcription factor, nuclear factor kappa B (NF-kappaB), which was persistently activated by cycloheximide but not by other agents after 24 hours indicating no role of NFkappaB in the RNase L-induction. |
1(0,0,0,1) | Details |
18362888 | Jeon YJ, Kim IK, Hong SH, Nan H, Kim HJ, Lee HJ, Masuda ES, Meyuhas O, Oh BH, Jung YK: Ribosomal protein S6 is a selective mediator of TRAIL-apoptotic signaling. Oncogene. 2008 Jul 17;27(31):4344-52. Epub 2008 Mar 24. TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is a potent inducer of apoptosis in tumor cells and holds a promise as a therapeutic agent against cancer. Reduction of rpS6 expression in Jurkat and HeLa cells attenuated apoptosis induced by TRAIL, but not those by other cell death signals, including tumor necrosis factor-alpha and cycloheximide, etoposide, doxorubicin, tunicamycin and staurosporine. |
1(0,0,0,1) | Details |
16405428 | Midwinter RG, Cheah FC, Moskovitz J, Vissers MC, Winterbourn CC: IkappaB is a sensitive target for oxidation by cell-permeable chloramines: inhibition of NF-kappaB activity by chloramine through oxidation. Biochem J. 2006 May 15;396(1):71-8. Oxidation by Gly-Cl prevented IkappaBalpha degradation in cells treated with TNFalpha (tumour necrosis factor alpha) and inhibited nuclear translocation of NF-kappaB. Reversion occurred in the presence of cycloheximide, but was prevented if thioredoxin reductase was inhibited, suggesting that it was due to endogenous sulphoxide reductase activity. |
1(0,0,0,1) | Details |
17545621 | Ivanov VN, Zhou H, Hei TK: Sequential treatment by ionizing radiation and arsenite dramatically accelerates TRAIL-mediated apoptosis of human melanoma cells. Cancer Res. 2007 Jun 1;67(11):5397-407. We show in the present study that gamma-irradiation, as well as alpha-particle exposure, dramatically increases the susceptibility of melanoma cells to recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis via up-regulation of surface TRAIL-receptor 1/receptor 2 (DR4/DR5) levels and to Fas ligand-mediated apoptosis via up-regulation of surface Fas levels. |
1(0,0,0,1) | Details |
18638274 | Shao H, Yi XM, Wells A: Epidermal growth factor protects fibroblasts from apoptosis via PI3 kinase and Rac signaling pathways. Wound Repair Regen. 2008 Jul-Aug;16(4):551-8. Interestingly, EGF prevention of apoptosis induced by tumor necrosis factor-alpha in the face of cycloheximide blockade of protein translation occurs via a different set of pathways as the simultaneous inhibition of extracellular signal-regulated kinase, Rac, and PI3K signaling did not eliminate EGF from rescuing fibroblasts in the face of this cytokine. |
0(0,0,0,0) | Details |
18406357 | Cullingford TE, Butler MJ, Marshall AK, Tham el L, Sugden PH, Clerk A: Differential regulation of Kruppel-like factor family transcription factor expression in neonatal rat cardiac myocytes: effects of endothelin-1, oxidative stress and cytokines. Biochim Biophys Acta. 2008 Jun;1783(6):1229-36. Epub 2008 Mar 25. All were regulated as immediate early genes (cycloheximide did not inhibit the increases in expression). |
0(0,0,0,0) | Details |
19492103 | Ito T, Oshita S, Nakabayashi T, Sun F, Kinjo M, Ohta N: Fluorescence lifetime images of green fluorescent protein in HeLa cells during TNF-alpha induced apoptosis. Photochem Photobiol Sci. 2009 Jun;8(6):763-7. Epub 2009 Apr 14. Fluorescence lifetime images of HeLa cells expressing enhanced green fluorescent protein (EGFP) have been measured as apoptosis is induced by tumor necrosis factor-alpha (TNF-alpha) in combination with cycloheximide. |
7(0,0,1,2) | Details |
18997433 | Nishimoto S, Goto Y, Morishige H, Shiraishi R, Doi M, Akiyama K, Yamauchi S, Sugahara T: Mode of action of the immunostimulatory effect of collagen from jellyfish. Biosci Biotechnol Biochem. 2008 Nov;72(11):2806-14. Epub 2008 Nov 7. The expression levels of immunoglobulin mRNAs in HB4C5 cells, and those of tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and transforming growth factor (TGF)-beta in hPBL were up-regulated by jellyfish collagen. This collagen also enhanced IgM production by translation-suppressed HB4C5 cells that had been treated with but was ineffective in accelerating IgM production by HB4C5 cells treated with cycloheximide. |
1(0,0,0,1) | Details |
19075022 | Lauer ME, Fulop C, Mukhopadhyay D, Comhair S, Erzurum SC, Hascall VC: Airway smooth muscle cells synthesize cable structures independent of inter-alpha-inhibitor heavy chain attachment. J Biol Chem. 2009 Feb 20;284(8):5313-23. Epub 2008 Dec 15. HC transfer has been shown to be mediated by the protein product of TSG-6 (tumor necrosis factor-stimulated gene 6). Functional cables were induced by cycloheximide in the confirmed absence of protein synthesis, with or without simultaneous treatment with poly (I,C). |
1(0,0,0,1) | Details |
15806306 | Tanaka F, Kawakami A, Tamai M, Nakamura H, Iwanaga N, Izumi Y, Arima K, Aratake K, Huang M, Kamachi M, Ida H, Origuchi T, Eguchi K: IFN-gamma/JAK/STAT pathway-induced inhibition of DR4 and DR5 expression on endothelial cells is cancelled by cycloheximide-sensitive mechanism: novel finding of cycloheximide-regulating death receptor expression. Int J Mol Med. 2005 May;15(5):833-9. The pathway of interferon gamma (IFN-gamma-induced suppression in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated endothelial cell apoptosis was investigated. rTRAIL triggered apoptosis of human umbilical vein endothelial cells (HUVECs) in a type II cell death manner. |
1(0,0,0,1) | Details |
17143556 | Lai YL, Yamaguchi M: Phytocomponent inhibits osteoclast-like cell formation in mouse bone marrow cultures. Int J Mol Med. 2007 Jan;19(1):123-8. The inhibitory effect of HCA (10 (-6) or 10 (-5) M) on RANKL plus M-CSF-induced osteoclast-like cell formation was not observed in the presence of cycloheximide (10 (-7) M), an inhibitor of protein synthesis in the transcriptional process, or 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (10 (-6) M), an inhibitor of transcription. The bone marrow cells were cultured for 7 days in alpha-minimal essential medium containing a bone-resorbing agent [parathyroid hormone (1-34)] (PTH), or tumor necrosis factor-alpha (TNF-alpha) in effective concentrations. |
1(0,0,0,1) | Details |
15649403 | Shimizu K, Watanabe K, Yamashita H, Abe M, Yoshimatsu H, Ohta H, Sonoda H, Sato Y: Gene regulation of a novel angiogenesis inhibitor, vasohibin, in endothelial cells. Biochem Biophys Res Commun. 2005 Feb 18;327(3):700-6. Actinomycin D did not alter the kinetics of vasohibin mRNA induction upon VEGF treatment, whereas cycloheximide completely abolished its induction. TNFalpha, IL1 and IFNgamma decreased VEGF-stimulated vasohibin expression. |
1(0,0,0,1) | Details |
15578574 | Yamaguchi M, Uchiyama S: Regucalcin stimulates osteoclast-like cell formation in mouse marrow cultures. J Cell Biochem. 2005 Mar 1;94(4):794-803. The effect of regucalcin on osteoclast-like cell formation was not significantly blocked in the presence of cycloheximide, an inhibitor of protein synthesis, or 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), an inhibitor of transcriptional activity. The effect of parathyroid hormone (10 (-7) M), (3) (10 (-7) M), (2) (10 (-5) M), or tumor necrosis factor-alpha (10 ng/ml) in increasing osteoclast-like cell formation was significantly enhanced in the presence of regucalcin (10 (-8) M). |
1(0,0,0,1) | Details |
18052213 | Pai T, Chen Q, Zhang Y, Zolfaghari R, Ross AC: Galactomutarotase and other myeloid cells. Biochemistry. 2007 Dec 25;46(51):15198-207. Epub 2007 Dec 4. The increase in GALM mRNA by RA was blocked by pretreating THP-1 cells with actinomycin D but not by cycloheximide. |
-related genes are rapidly induced by in human 0(0,0,0,0) | Details |
16299053 | Busch CJ, Liu H, Graveline AR, Bloch KD: phosphodiesterase 4B expression in rat pulmonary artery smooth muscle cells. Am J Physiol Lung Cell Mol Physiol. 2006 Apr;290(4):L747-L753. Epub 2005 Nov 18. The GSNO-induced increase in PDE4B mRNA levels was blocked by actinomycin D but augmented by cycloheximide. |
induces 0(0,0,0,0) | Details |
19128821 | Di Stefano R, Barsotti MC, Armani C, Santoni T, Lorenzet R, Balbarini A, Celi A: Human peripheral blood endothelial progenitor cells synthesize and express functionally active tissue factor. Thromb Res. 2009 Apr;123(6):925-30. Epub 2009 Jan 6. Both 5,6-dichloro-beta D-ribofuranosyl-benzimidazole and cycloheximide prevented the expression of procoagulant activity. |
0(0,0,0,0) | Details |
17265482 | Kirino Y, Takeno M, Murakami S, Kobayashi M, Kobayashi H, Miura K, Ideguchi H, Ohno S, Ueda A, Ishigatsubo Y: Tumor necrosis factor alpha acceleration of inflammatory responses by down-regulating heme oxygenase 1 in human peripheral monocytes. Arthritis Rheum. 2007 Feb;56(2):464-75. Actinomycin D and cycloheximide were used to monitor the stability of mRNA and protein. |
7(0,0,0,7) | Details |
15659777 | Boulday G, Fitau J, Coupel S, Soulillou JP, Charreau B: Exogenous tissue inhibitor of metalloproteinase-1 promotes endothelial cell survival through activation of the phosphatidylinositol 3-kinase/Akt pathway. Ann N Y Acad Sci. 2004 Dec;1030:28-36. We demonstrate that exogenous, recombinant, TIMP-1 efficiently prevents apoptosis induced by TNFalpha in cycloheximide-sensitized ECs. |
7(0,0,1,2) | 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: 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 treatment sensitized RKO cells to tumor necrosis factor alpha-related apoptosis-inducing ligand-induced apoptosis. |
and 1(0,0,0,1) | Details |
18973758 | Frey MR, Edelblum KL, Mullane MT, Liang D, Polk DB: The ErbB4 growth factor receptor is required for colon epithelial cell survival in the presence of TNF. Gastroenterology. 2009 Jan;136(1):217-26. Epub 2008 Sep 25. ErbB4 siRNA sensitized cells to TNF-stimulated apoptosis, while over expression blocked apoptosis induced by TNF plus cycloheximide. Mice were subjected to dextran (DSS, 3%) colitis or injected with tumor necrosis factor (TNF), and ErbB4 expression was quantified by immunohistochemistry and Western blot. |
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. |
0(0,0,0,0) | Details |
17442733 | Zhang AH, Rao JN, Zou T, Liu L, Marasa BS, Xiao L, Chen J, Turner DJ, Wang JY: p53-dependent NDRG1 expression induces inhibition of intestinal epithelial cell proliferation but not apoptosis after polyamine depletion. Am J Physiol Cell Physiol. 2007 Jul;293(1):C379-89. Epub 2007 Apr 18. However, overexpression of NDRG1 failed to directly induce cell death and to alter susceptibility to apoptosis induced by tumor necrosis factor-alpha/cycloheximide. |
0(0,0,0,0) | Details |
18180277 | Stojanov S, Dejaco C, Lohse P, Huss K, Duftner C, Belohradsky BH, Herold M, Schirmer M: Clinical and functional characterisation of a novel TNFRSF1A c.605T> A/V173D cleavage site mutation associated with tumour necrosis factor receptor-associated periodic fever syndrome (TRAPS), cardiovascular complications and excellent response to etanercept treatment. Ann Rheum Dis. 2008 Sep;67(9):1292-8. Epub 2008 Jan 7. Apoptosis of PBMCs was studied by stimulation with TNFalpha in the presence of cycloheximide and annexin V staining. |
7(0,0,1,2) | Details |
15843903 | Engbers-Buijtenhuijs P, Kamphuis M, van der Sluijs Veer G, Haanen C, Poot AA, Feijen J, Vermes I: A novel time resolved fluorometric assay of anoikis using Europium-labelled Annexin V in cultured adherent cells. Apoptosis. 2005 Mar;10(2):429-37. Anoikis was induced with tumor necrosis factor-alpha/cycloheximide and three cell fractions of the cell cultures were prepared and analysed. |
6(0,0,1,1) | Details |
16966373 | Gyrd-Hansen M, Farkas T, Fehrenbacher N, Bastholm L, Hoyer-Hansen M, Elling F, Wallach D, Flavell R, Kroemer G, Nylandsted J, Jaattela M: Apoptosome-independent activation of the lysosomal cell death pathway by caspase-9. Mol Cell Biol. 2006 Nov;26(21):7880-91. Epub 2006 Sep 11. By using a large panel of genetically modified murine embryonic fibroblasts, we show here that, in response to tumor necrosis factor (TNF), caspase-8 cleaves and activates caspase-9 in an apoptosome-independent manner. |
1(0,0,0,1) | Details |
16883635 | Lee KH, Choi EM: Rubus coreanus Miq. extract promotes osteoblast differentiation and inhibits bone-resorbing mediators in MC3T3-E1 cells. Am J Chin Med. 2006;34(4):643-54. The effect of RCE (50 microg/ml) in increasing cell viability, ALP activity, and collagen content was prevented by the presence of 10 (-6) M cycloheximide and 10 (-6) M tamoxifen, suggesting that RCE's effect results from a newly synthesized protein component and might be partly involved in action. Treatment with RCE (10approximately50 microg/ml) decreased the 0.2 mM H (2) O (2)-induced apoptosis and production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and (NO) in osteoblasts. |
1(0,0,0,1) | Details |
18497737 | He F, Doucet JA, Stephens JM: Caspase-mediated degradation of PPARgamma proteins in adipocytes. . Obesity (Silver Spring). 2008 Aug;16(8):1735-41. Epub 2008 May 22. RESULTS: We observed that TNFalpha can induce a caspase-mediated degradation of PPARgamma proteins in the presence of cycloheximide. |
114(1,2,2,4) | Details |
15629764 | Ebert AD, Chen F, He X, Cryns VL, Bohn MC: A tetracycline-regulated adenovirus encoding dominant-negative caspase-9 is regulated in rat brain and protects against neurotoxin-induced cell death in vitro, but not in vivo. Exp Neurol. 2005 Feb;191 Suppl 1:S80-94. We next observed that Casp9DN gene delivery significantly protected against TNFalpha and cycloheximide-induced chromatin condensation in HeLa cells and prevented chromatin condensation and the appearance of the early apoptotic marker annexin V in (6-OHDA) treated MN9D cells, a dopaminergic cell line. |
6(0,0,1,1) | Details |
18030348 | Thedieck K, Polak P, Kim ML, Molle KD, Cohen A, Jeno P, Arrieumerlou C, Hall MN: PRAS40 and PRR5-like protein are new mTOR interactors that regulate apoptosis. PLoS One. 2007 Nov 21;2(11):e1217. HeLa cells in which PRAS40 was knocked down were protected against induction of apoptosis by TNFalpha and cycloheximide. |
6(0,0,1,1) | 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. RESEARCH DESIGN AND METHODS: We isolated islets from mice lacking Bid, Bax, or Bak and those overexpressing Bcl-2 and exposed them to Fas ligand, tumor necrosis factor (TNF)-alpha, and proinflammatory cytokines or cytotoxic stimuli that activate the mitochondrial apoptotic pathway (staurosporine, etoposide, gamma-radiation, tunicamycin, and thapsigargin). Bid-deficient islets were also resistant to apoptosis induced by TNF-alpha plus cycloheximide and were partially resistant to proinflammatory cytokine-induced death. |
1(0,0,0,1) | Details |
15640153 | Pillinger MH, Marjanovic N, Kim SY, Scher JU, Izmirly P, Tolani S, Dinsell V, Lee YC, Blaser MJ, Abramson SB: Matrix metalloproteinase secretion by gastric epithelial cells is regulated by E prostaglandins and MAPKs. J Biol Chem. 2005 Mar 18;280(11):9973-9. Epub 2005 Jan 7. Tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and epidermal growth factor (EGF) stimulated gastric cell MMP-1 secretion, indicating that MMP-1 secretion occurs in inflammatory as well as non-inflammatory situations. |
1(0,0,0,1) | Details |
18522940 | Hellwig CT, Kohler BF, Lehtivarjo AK, Dussmann H, Courtney MJ, Prehn JH, Rehm M: Real time analysis of tumor necrosis factor-related apoptosis-inducing ligand/cycloheximide-induced caspase activities during apoptosis initiation. J Biol Chem. 2008 Aug 1;283(31):21676-85. Epub 2008 Jun 3. |
82(1,1,1,2) | Details |
16487927 | Saeki M, Irie Y, Ni L, Yoshida M, Itsuki Y, Kamisaki Y: Monad, a WD40 repeat protein, promotes apoptosis induced by TNF-alpha. Biochem Biophys Res Commun. 2006 Apr 7;342(2):568-72. Epub 2006 Feb 10. Overexpression of Monad in HEK293 cells potentiated apoptosis and caspase-3 activation induced by tumor necrosis factor-alpha and cycloheximide. |
81(1,1,1,1) | Details |
17101148 | Reil JC, Gilles S, Zahler S, Brandl A, Drexler H, Hultner L, Matrisian LM, Welsch U, Becker BF: Insights from knock-out models concerning postischemic release of TNFalpha from isolated mouse hearts. J Mol Cell Cardiol. 2007 Jan;42(1):133-41. Epub 2006 Nov 13. We employed hearts of various mice knock-out strains (interleukin-6 (-/-), matrix metalloprotease-7 (-/-), mast-cell deficient WBB6F1-Kit (W)/Kit (W-v), TNF-R1 (-/-)) and wildtype mice, the latter perfused without and with infusion of cycloheximide or TNFalpha-cleaving-enzyme inhibitor (TAPI-2). |
40(0,1,1,10) | Details |
16478887 | Mitchell JW, Baik N, Castellino FJ, Miles LA: Plasminogen inhibits TNFalpha-induced apoptosis in monocytes. . Blood. 2006 Jun 1;107(11):4383-90. Epub 2006 Feb 14. Plasminogen treatment also markedly reduced internucleosomal DNA fragmentation and reduced levels of active caspase 3, caspase 8, and caspase 9 induced by TNFalpha or by cycloheximide. |
38(0,1,2,3) | Details |
19302817 | N'Diaye M, Le Ferrec E, Kronenberg F, Dieplinger H, Le Vee M, Fardel O: TNFalpha- and NF-kappaB-dependent induction of the chemokine CCL1 in human macrophages exposed to the atherogenic lipoprotein (a). Life Sci. 2009 Mar 27;84(13-14):451-7. Epub 2009 Feb 2. KEY FINDINGS: Using the AhR antagonist alpha-napthtoflavone, the translational inhibitor cycloheximide and anti-tumor necrosis factor alpha (TNFalpha) neutralizing antibodies, we demonstrated that Lp (a)-mediated mRNA induction of CCL1 occurs in an AhR-independent manner and requires de novo protein synthesis of TNFalpha. |
34(0,1,1,4) | Details |
15767410 | Hsu WL, Saffran HA, Smiley JR: Herpes simplex virus infection stabilizes cellular IEX-1 mRNA. J Virol. 2005 Apr;79(7):4090-8. This truncated transcript was also detected (albeit at lower levels) in cells infected with vhs mutants and in uninfected cells, where it increased in abundance in response to tumor necrosis factor alpha, cycloheximide, and puromycin. |
6(0,0,1,1) | Details |
17003650 | Li Y, Li G, Dong W, Chen J, Lu D, Tan J: Transplantation of rat islets transduced with human heme oxygenase-1 gene using adenovirus vector. Pancreas. 2006 Oct;33(3):280-6. Flow cytometry was used to detect apoptotic cells after induction by recombinant human tumor necrosis factor-alpha (rTNF-alpha) and cycloheximide (CHX) for 48 hours. |
6(0,0,1,1) | Details |
16411808 | Engbers-Buijtenhuijs P, Buttafoco L, Poot AA, Geelkerken RH, Feijen J, Vermes I: Analysis of the balance between proliferation and apoptosis of cultured vascular smooth muscle cells for tissue-engineering applications. Tissue Eng. 2005 Nov-Dec;11(11-12):1631-9. Human vascular smooth muscle cells (VSMCs) were cultured either on gelatin-coated tissue culture polystyrene or in three-dimensional porous scaffolds composed of insoluble collagen and elastin. mRNA concentrations of cyclin E, as a marker of proliferation, and of tissue transglutaminase (tTG) as a marker of apoptosis, quantified by a real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and normalized to porphobilinogen deaminase mRNA concentrations, were analyzed. tTG mRNA expression levels were increased when apoptosis was induced by tumor necrosis factor-alpha in combination with cycloheximide or by culturing the cells in serum-free culture medium. |
6(0,0,1,1) | Details |
19180575 | Ni L, Saeki M, Xu L, Nakahara H, Saijo M, Tanaka K, Kamisaki Y: RPAP3 interacts with Reptin to regulate UV-induced phosphorylation of H2AX and DNA damage. J Cell Biochem. 2009 Apr 1;106(5):920-8. We have previously reported that Monad, a novel WD40 repeat protein, potentiates apoptosis induced by tumor necrosis factor-alpha and cycloheximide. |
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. TNF-alpha-induced JNK phosphorylation was sustained in the presence of cycloheximide, which was accompanied by accelerated neutrophil apoptosis. |
1(0,0,0,1) | Details |
15535971 | Kamiya S, Kawaguchi T, Hasebe S, Kamiya N, Saito Y, Miura S, Wada S, Yajima H, Katayama T, Fukai F: A fibronectin fragment induces tumor necrosis factor production of rat basophilic leukemia cells. Biochim Biophys Acta. 2004 Nov 18;1675(1-3):87-94. The TNF-alpha secretion was abrogated by treatment of RBL-2H3 cells with cycloheximide, indicating the de novo synthesis of TNF-alpha, but not with polymyxin B, excluding the possible TNF-alpha induction by some contaminated lipopolysaccharides. |
1(0,0,0,1) | Details |
16931628 | Fas SC, Baumann S, Zhu JY, Giaisi M, Treiber MK, Mahlknecht U, Krammer PH, Li-Weber M: Wogonin sensitizes resistant malignant cells to TNFalpha- and TRAIL-induced apoptosis. Blood. 2006 Dec 1;108(12):3700-6. Epub 2006 Aug 24. To overcome this problem in vitro, specific NF-kappaB inhibitors or transcription or protein synthesis inhibitors such as actinomycin D and cycloheximide are usually used in combination to increase TNFalpha killing of tumor cells. |
36(0,1,1,6) | Details |
16569452 | Sakurai T, Itoh K, Higashitsuji H, Nonoguchi K, Liu Y, Watanabe H, Nakano T, Fukumoto M, Chiba T, Fujita J: Cirp protects against tumor necrosis factor-alpha-induced apoptosis via activation of extracellular signal-regulated kinase. Biochim Biophys Acta. 2006 Mar;1763(3):290-5. Epub 2006 Mar 20. In BALB/3T3 cells treated with tumor necrosis factor (TNF)-alpha and cycloheximide, the down-shift in temperature from 37 degrees C to 32 degrees C increased the expression of Cirp and suppressed the apoptosis. |
32(0,1,1,2) | Details |
17042977 | Li YX, Li G, Dong WP, Lu DR, Tan JM: Protection of human islets from induction of apoptosis and improved islet function with HO-1 gene transduction. Chin Med J. 2006 Oct 5;119(19):1639-45. Flow cytometry was used to detect apoptotic cells in the HO-1 group and in the control group after induction by recombinant human tumor necrosis factor-alpha (rTNFalpha) and cycloheximide (CHX) for 48 hours. |
6(0,0,1,1) | Details |
19648110 | King EM, Holden NS, Gong W, Rider CF, Newton R: Inhibition of NF-kappaB-dependent transcription by MKP-1: transcriptional repression by glucocorticoids occurring via p38 MAPK. J Biol Chem. 2009 Sep 25;284(39):26803-15. Epub 2009 Jul 31. This correlates with reduced TNFalpha-stimulated p38 MAPK phosphorylation. |
5(0,0,0,5) | Details |
16446372 | Caruso JA, Mathieu PA, Joiakim A, Zhang H, Reiners JJ Jr: Aryl hydrocarbon receptor modulation of tumor necrosis factor-alpha-induced apoptosis and lysosomal disruption in a hepatoma model that is caspase-8-independent. J Biol Chem. 2006 Apr 21;281(16):10954-67. Epub 2006 Jan 30. |
4(0,0,0,4) | Details |
16637064 | Choi W, Proctor L, Xia Q, Feng Y, Gerner EW, Chiao PJ, Hamilton SR, Zhang W: Inactivation of IkappaB contributes to transcriptional activation of / N (1)-acetyltransferase. Mol Carcinog. 2006 Sep;45(9):685-93. Luciferase reporter gene assay showed that SSAT promoter constructs containing the two putative NFkappaB binding elements responded to CHX as well as TNFalpha, whereas the promoter without the two sites did not. |
1(0,0,0,1) | Details |
17989354 | Wang P, Julian JA, Carson DD: The MUC1 HMFG1 glycoform is a precursor to the 214D4 glycoform in the human uterine epithelial cell line, HES. Biol Reprod. 2008 Feb;78(2):290-8. Epub 2007 Nov 7. In response to tumor necrosis factor stimulation, accumulation of the HMFG1-reactive forms preceded that of the 214D4-reactive forms. Following inhibition of protein synthesis by cycloheximide, HMFG1-reactive species were lost rapidly (metabolic half-life [T (1/2)] = 20 min), while there was no change in the level of the 214D4-reactive forms even after 80 min. |
1(0,0,0,1) | Details |
17435549 | Turner DJ, Alaish SM, Zou T, Rao JN, Wang JY, Strauch ED: Bile salts induce resistance to apoptosis through NF-kappaB-mediated XIAP expression. Ann Surg. 2007 Mar;245(3):415-25. Exposure of normal intestinal epithelial cells (IEC-6) to the conjugated bile salts taurodeoxycholate (TDCA) and (TCDCA) resulted in an increase in resistance to tumor necrosis factor (TNF)-alpha and cycloheximide (CHX)-induced apoptosis, and NF-kappaB activation. |
31(0,1,1,1) | Details |
17324936 | Saeki M, Irie Y, Ni L, Itsuki Y, Terao Y, Kawabata S, Kamisaki Y: Calcineurin potentiates the activation of procaspase-3 by accelerating its proteolytic maturation. J Biol Chem. 2007 Apr 20;282(16):11786-94. Epub 2007 Feb 26. Overexpression of calcineurin B in HEK293 cells potentiated processing of caspase-3 and apoptosis triggered by tumor necrosis factor-alpha and cycloheximide treatment. |
31(0,1,1,1) | Details |
15641051 | Franchimont N, Lambert C, Huynen P, Ribbens C, Relic B, Chariot A, Bours V, Piette J, Merville MP, Malaise M: Interleukin-6 receptor shedding is enhanced by interleukin-1beta and tumor necrosis factor alpha and is partially mediated by tumor necrosis factor alpha-converting enzyme in osteoblast-like cells. Arthritis Rheum. 2005 Jan;52(1):84-93. This effect was not influenced by cycloheximide or 5,6-dichlorobenzimidazole riboside but was markedly inhibited by the chelator EGTA and by the TACE and matrix metalloproteinase inhibitor hydroxamate (Ru36156). |
4(0,0,0,4) | Details |
16826536 | Chan G, Guilbert LJ: Ultraviolet-inactivated human cytomegalovirus induces placental syncytiotrophoblast apoptosis in a Toll-like receptor-2 and tumour necrosis factor-alpha dependent manner. J Pathol. 2006 Sep;210(1):111-20. ST cultures challenged with UV-HCMV increased transcription and secretion of the inflammatory cytokines tumour necrosis factor alpha (TNFalpha) and interleukin-8, and antibody to TNFalpha inhibited UV-HCMV-induced apoptosis. Treatment with cycloheximide, an inhibitor of protein translation, did not reduce UV-HCMV-induced TNFalpha gene transcription, indicating that upregulation was independent of de novo protein synthesis. |
3(0,0,0,3) | Details |
16982682 | Smoak K, Cidlowski JA: Glucocorticoids regulate tristetraprolin synthesis and posttranscriptionally regulate tumor necrosis factor alpha inflammatory signaling. Mol Cell Biol. 2006 Dec;26(23):9126-35. Epub 2006 Sep 18. Glucocorticoid induction of TTP mRNA is also blocked by actinomycin D but not by cycloheximide, suggesting a transcriptional mechanism which has been confirmed by transcription run-on experiments. |
2(0,0,0,2) | Details |
18086809 | Stone MK, Kolling GL, Lindner MH, Obrig TG: p38 mitogen-activated protein kinase mediates lipopolysaccharide and tumor necrosis factor alpha induction of shiga toxin 2 sensitivity in human umbilical vein endothelial cells. Infect Immun. 2008 Mar;76(3):1115-21. Epub 2007 Dec 17. Cell viability assays indicated that the p38 mitogen-activated protein kinase (MAPK) inhibitors SB202190 and SB203580 and the general protein synthesis inhibitor cycloheximide inhibited both the LPS and TNF-alpha sensitization of HUVEC to Stx2, while all other inhibitors tested did not inhibit this sensitization. |
2(0,0,0,2) | Details |
16714014 | Mormina ME, Thakur S, Molleman A, Whelan CJ, Baydoun AR: Cannabinoid signalling in TNF-alpha induced IL-8 release. Eur J Pharmacol. 2006 Jul 1;540(1-3):183-90. Epub 2006 May 5. Release of IL-8 induced by tumor necrosis factor-alpha (TNF-alpha) was determined by enzyme-linked immunosorbent assay (ELISA). |
1(0,0,0,1) | Details |
16368179 | Ito K, Kiyosawa N, Kumagai K, Manabe S, Matsunuma N, Yamoto T: Molecular mechanism investigation of cycloheximide-induced hepatocyte apoptosis in rat livers by morphological and microarray analysis. Toxicology. 2006 Feb 15;219(1-3):175-86. Epub 2005 Dec 20. The hepatic mRNA levels of proinflammatory genes, such as TNFalpha, IL-1alpha and beta, were also increased 1 and 2h after the CHX treatment, supposedly mediated by the activated Kupffer cells engulfing the apoptotic hepatocytes. |
1(0,0,0,1) | Details |
17804813 | Xiao L, Rao JN, Zou T, Liu L, Marasa BS, Chen J, Turner DJ, Zhou H, Gorospe M, Wang JY: Polyamines regulate the stability of activating transcription factor-2 mRNA through RNA-binding protein HuR in intestinal epithelial cells. Mol Biol Cell. 2007 Nov;18(11):4579-90. Epub 2007 Sep 5. Furthermore, inhibition of ATF-2 expression prevented the increased resistance of polyamine-deficient cells to apoptosis induced by treatment with tumor necrosis factor-alpha and cycloheximide. |
31(0,1,1,1) | Details |
19233135 | Kato T, Ikemoto M, Hato F, Kitagawa S: Granule swelling and cleavage of mitogen-activated protein kinases in human neutrophils undergoing apoptosis. Biochem Biophys Res Commun. 2009 Apr 10;381(3):434-8. Epub 2009 Feb 20. Extracellular signal-regulated kinase and p38 have been shown to be cleaved in human neutrophils undergoing apoptosis induced by tumor necrosis factor-alpha and cycloheximide. |
31(0,1,1,1) | Details |
16432762 | Xia Y, Novak R, Lewis J, Duckett CS, Phillips AC: Xaf1 can cooperate with TNFalpha in the induction of apoptosis, independently of interaction with XIAP. Mol Cell Biochem. 2006 Jun;286(1-2):67-76. Epub 2006 Jan 24. |
2(0,0,0,2) | Details |
16835229 | Fukui N, Ikeda Y, Ohnuki T, Hikita A, Tanaka S, Yamane S, Suzuki R, Sandell LJ, Ochi T: Pro-inflammatory cytokine tumor necrosis factor-alpha induces bone morphogenetic protein-2 in chondrocytes via mRNA stabilization and transcriptional up-regulation. J Biol Chem. 2006 Sep 15;281(37):27229-41. Epub 2006 Jul 11. The results of nuclear run-off assay and cycloheximide treatment consistently indicated that ATDC5 cells acquire the capacity to synthesize BMP-2 mRNA in the nuclei during the differentiation process. |
2(0,0,0,2) | Details |
16166516 | Covert MW, Leung TH, Gaston JE, Baltimore D: Achieving stability of lipopolysaccharide-induced NF-kappaB activation. Science. 2005 Sep 16;309(5742):1854-7. The activation dynamics of the transcription factor NF-kappaB exhibit damped oscillatory behavior when cells are stimulated by tumor necrosis factor-alpha (TNFalpha) but stable behavior when stimulated by lipopolysaccharide (LPS). |
2(0,0,0,2) | Details |
17304101 | Pearl-Yafe M, Fabian I, Halperin D, Flatau E, Werber S, Shalit I: Interferon-gamma and bacterial lipopolysaccharide act synergistically on human neutrophils enhancing interleukin-8, interleukin-1beta, tumor necrosis factor-alpha, and interleukin-12 p70 secretion and phagocytosis via upregulation of toll-like receptor 4. Shock. 2007 Mar;27(3):226-31. Using the protein synthesis inhibitor cycloheximide and measuring the expression of CD35 in neutrophils stimulated with IFN-gamma and LPS alone or in combination, we could demonstrate that IFN-gamma enhances TLR4 by de novo protein synthesis, whereas the addition of LPS acts synergistically by enhancing vesicular mobilization to the cell surface. |
2(0,0,0,2) | Details |
16157236 | Su SJ, Huang LW, Pai LS, Liu HW, Chang KL: activates human monocyte and induces cytokine expression and inhibits macrophage migration inhibitory factor expression. Nutrition. 2005 Oct;21(10):994-1002. METHODS: Human monocytes were treated in vitro with a variety of concentrations that ranged from physiologic concentration to higher than pathophysiologic concentration, and we analyzed their expressions of inflammatory cytokines, including tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interleukin-8, interleukin-12, and migration inhibitory factor. |
at pathophysiologic concentrations 2(0,0,0,2) | Details |
17614795 | Aufiero B, Guo M, Young C, Duanmu Z, Talwar H, Lee HK, Murakawa GJ: Staphylococcus aureus induces the expression of tumor necrosis factor-alpha in primary human keratinocytes. Int J Dermatol. 2007 Jul;46(7):687-94. |
2(0,0,0,2) | Details |
15586230 | Vigneswaran N, Wu J, Nagaraj N, Adler-Storthz K, Zacharias W: Differential susceptibility of metastatic and primary oral cancer cells to TRAIL-induced apoptosis. Int J Oncol. 2005 Jan;26(1):103-12. TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) preferentially induces apoptosis of cancer cells without toxicity in normal cells. The protein synthesis inhibitor cycloheximide markedly increased the TRAIL sensitivity of these cell lines, whereas the CB-specific chemical inhibitor CA-074 markedly reduced the sensitivity of primary OC cells to TRAIL. |
1(0,0,0,1) | Details |
17194804 | Lee SY, Cherla RP, Tesh VL: Simultaneous induction of apoptotic and survival signaling pathways in macrophage-like THP-1 cells by Shiga toxin 1. Infect Immun. 2007 Mar;75(3):1291-302. Epub 2006 Dec 28. Finally, the protein synthesis inhibitors Stx1 and anisomycin triggered limited apoptosis and prolonged JNK and p38 MAPK activation, while macrophage-like cells treated with cycloheximide remained viable and showed transient activation of MAPKs. Differentiated THP-1 cells expressed tumor necrosis factor receptors and membrane-associated tumor necrosis factor alpha (TNF-alpha) and produced soluble TNF-alpha after exposure to Stx1. |
1(0,0,0,1) | Details |
18196969 | Pyo JO, Nah J, Kim HJ, Lee HJ, Heo J, Lee H, Jung YK: Compensatory activation of ERK1/2 in Atg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death. Autophagy. 2008 Apr 1;4(3):315-21. Epub 2008 Jan 7. On the contrary, Atg5-/- MEFs were as sensitive to tumor necrosis factor (TNF)-alpha and cycloheximide as WT cells, and were more sensitive to cell death triggered by amino acid-deprivation than WT MEFs. |
31(0,1,1,1) | Details |
16551274 | Marasa BS, Rao JN, Zou T, Liu L, Keledjian KM, Zhang AH, Xiao L, Chen J, Turner DJ, Wang JY: Induced TRPC1 expression sensitizes intestinal epithelial cells to apoptosis by inhibiting NF-kappaB activation through Ca2+ influx. Biochem J. 2006 Jul 1;397(1):77-87. The expression of TRPC1 induced by stable transfection of IEC-6 cells with the wild-type TRPC1 gene (IEC-TRPC1 cells) increased Ca2+ influx after Ca2+ store depletion and repressed NF-kappaB transactivation, which was associated with an increase in susceptibility to apoptosis induced by exposure to TNFalpha (tumour necrosis factor-alpha) plus CHX (cycloheximide) (TNF-alpha/CHX), or STS (staurosporine). |
31(0,1,1,1) | Details |
16790802 | Bennouna S, Sukhumavasi W, Denkers EY: Toxoplasma gondii inhibits toll-like receptor 4 ligand-induced mobilization of intracellular tumor necrosis factor alpha to the surface of mouse peritoneal neutrophils. Infect Immun. 2006 Jul;74(7):4274-81. In contrast to intermediate inhibitory effects in nontreated neutrophils, T. gondii induced a complete blockade in LPS-induced surface TNF-alpha expression in the presence of the protein synthesis inhibitor cycloheximide. |
2(0,0,0,2) | Details |
17583676 | Kamachi M, Aramaki T, Tanimura S, Ichinose K, Fujikawa K, Iwamoto N, Yoshizaki A, Ida H, Kawakami A, Kohno M, Eguchi K: Activation of protein phosphatase causes alternative splicing of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL): potential effect on immune surveillance. Biochem Biophys Res Commun. 2007 Aug 17;360(1):280-5. Epub 2007 Jun 15. Etoposide and cycloheximide induced alternative splicing, whereas staurosporine (a broad kinase inhibitor) blocked both constitutive and alternative splicing. |
2(0,0,0,2) | 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. |
2(0,0,0,2) | Details |
17014691 | Fernandes PA, Cecon E, Markus RP, Ferreira ZS: Effect of TNF-alpha on the pineal gland: basis for a 'feedback' of the immune response on circadian timing. J Pineal Res. 2006 Nov;41(4):344-50. Here we analyzed the effect of tumor necrosis factor-alpha (TNF-alpha) and on the transcription of the Aa-nat, hiomt and 14-3-3 protein genes in denervated pineal glands of rats stimulated for 5 hr with using real-time reverse transcription-polymerase chain reaction. In fact, a protein (s) transcribed, later on, as shown by cycloheximide, was responsible for the reversal of the inhibition of Aa-nat transcription. |
synthetic pathway in the rat 1(0,0,0,1) | Details |
15855330 | Mastrandrea LD, Sessanna SM, Laychock SG: production in rat pancreatic islets and INS-1 cells: response to cytokines. Diabetes. 2005 May;54(5):1429-36. SPHK activity increased in INS-1 cell homogenates treated with interleukin-1beta (IL-1beta) or tumor necrosis factor-alpha (TNF-alpha), and responses were additive. Cytokines increased endogenous S1P biosynthesis in 32P (i)-prelabeled INS-1 cells, and cycloheximide inhibited the response after 8 h, suggesting that protein synthesis mediated the response. |
kinase activity and 1(0,0,0,1) | Details |
18729741 | Shizu M, Itoh Y, Sunahara R, Chujo S, Hayashi H, Ide Y, Takii T, Koshiko M, Chung SW, Hayakawa K, Miyazawa K, Hirose K, Onozaki K: Cigarette smoke condensate upregulates the gene and protein expression of proinflammatory cytokines in human fibroblast-like synoviocyte line. J Interferon Cytokine Res. 2008 Aug;28(8):509-21. Cycloheximide treatment indicated that the augmenting effect of CSC on IL-1alpha, IL-1beta and IL-8, but not IL-6 and CYP1A1, mRNA expression requires de novo protein synthesis. CSC also induced cytokines at protein levels and further augmented the effects of tumor necrosis factor alpha on induction of these cytokines at both mRNA and protein levels. |
1(0,0,0,1) | Details |
16988256 | Dennis VA, Jefferson A, Singh SR, Ganapamo F, Philipp MT: Interleukin-10 anti-inflammatory response to Borrelia burgdorferi, the agent of Lyme disease: a possible role for suppressors of cytokine signaling 1 and 3. Infect Immun. 2006 Oct;74(10):5780-9. Neither endogenous IL-10 nor the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdorferi and its lipoproteins, indicating that the expression of other genes is not required. This temporally correlated with the IL-10-mediated inhibition of the inflammatory cytokines IL-1beta, IL-6, IL-12p40, IL-18, and tumor necrosis factor alpha. |
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17240354 | Sato F, Imaizumi T, Sashinami H, Yoshida H, Kusumi T, Mori F, Wakabayashi K, Nakane A, Satoh K, Kijima H: Upregulation of vascular endothelial growth factor by heat-killed Listeria monocytogenes in macrophages. Biochem Biophys Res Commun. 2007 Mar 9;354(2):608-12. Epub 2007 Jan 16. Pretreatment of cells with cycloheximide, a protein synthesis inhibitor, inhibited the induction of VEGF mRNA by HKLM. Induction of VEGF by HKLM was partially inhibited by treatment of cells with SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor, or a neutralizing antibody against tumor necrosis factor-alpha (TNF-alpha). |
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17337591 | Fernandez-Velasco M, Ruiz-Hurtado G, Hurtado O, Moro MA, Delgado C: TNF-alpha downregulates transient outward myocytes through iNOS overexpression and oxidant species generation. Am J Physiol Heart Circ Physiol. 2007 Jul;293(1):H238-45. Epub 2007 Mar 2. Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that has been implicated in the pathogenesis of heart failure. We have also demonstrated that the reduction of I (to) density induced by TNF-alpha was prevented by the selective inducible synthase (iNOS) inhibitor 1400-W, the protein synthesis inhibitor cycloheximide, the antioxidant and the superoxide dismutase mimetic (III) tetrakis (4- |
current in rat ventricular 1(0,0,0,1) | Details |
17584970 | Ramana KV, Tammali R, Reddy AB, Bhatnagar A, Srivastava SK: Aldose reductase-regulated tumor necrosis factor-alpha production is essential for high -induced vascular smooth muscle cell growth. Endocrinology. 2007 Sep;148(9):4371-84. Epub 2007 Jun 21. The increase in TNF-alpha production was prevented by actinomycin D and cycloheximide, indicating transcriptional activation of TNF-alpha gene. |
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18387309 | Doszczak M, Pierzchalski A, Grzenkowicz J, Stasilojc G, Bigda JJ: Cytocidal effect of interleukin 1 (IL-1) on HeLa cells is mediated by both soluble and transmembrane tumor necrosis factor (TNF). Cytokine. 2008 May;42(2):243-55. Epub 2008 Apr 1. We found that the pattern of IL-1-induced cell death shares significant similarities with the effect of tumor necrosis factor (TNF) in these cells. |
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15943580 | Caruso JA, Mathieu PA, Reiners JJ Jr: Sphingomyelins suppress the targeted disruption of lysosomes/endosomes by the photosensitizer NPe6 during photodynamic therapy. Biochem J. 2005 Dec 1;392(Pt 2):325-34. These results suggest that exogenously added 3-O-MeSM is trafficked to and stabilizes late endosomes/lysosomes against oxidant-induced damage, and further implicate a role for lysosomal proteases in the apoptotic processes initiated by TNFalpha and lysosomal photosensitizers. |
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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. A systematic study was undertaken to characterize the role of APO 2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (APO2L/TRAIL) and Fas ligand (FasL) together with the expression of several anti- or proapoptotic proteins in the down-regulation of normal human T cell responses. 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. |
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18065493 | Locklin RM, Federici E, Espina B, Hulley PA, Russell RG, Edwards CM: Selective targeting of death receptor 5 circumvents resistance of MG-63 osteosarcoma cells to TRAIL-induced apoptosis. Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3219-28. Epub 2007 Dec 7. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a tumor necrosis factor superfamily member, targets death receptors and selectively kills malignant cells while leaving normal cells unaffected. We show that TRAIL activates the canonical caspase-dependent pathway, whereas treatment with cycloheximide increases the sensitivity of MG-63 cells to TRAIL and anti-DR5 and can also sensitize hPOB-tert cells to both agents. |
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19800419 | Hwangbo C, Lee HS, Park J, Choe J, Lee JH: The anti-inflammatory effect of tussilagone, from Tussilago farfara, is mediated by the induction of heme oxygenase-1 in murine macrophages. Int Immunopharmacol. 2009 Dec;9(13-14):1578-84. Epub 2009 Oct 1. TSL-mediated HO-1 protein induction was not inhibited by treatment with actinomycin D, a transcriptional inhibitor, but by cycloheximide, a translational inhibitor. Consistent with the notion that HO-1 has anti-inflammatory properties, TSL inhibited the production of (NO), tumor necrosis factor (TNF)-alpha, and as well as inducible synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and murine peritoneal macrophages. |
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15722640 | Park CS, Choi EN, Kim JS, Choi YS, Rhim TY, Chang HS, Chung IY: Interferon-gamma inhibits in vitro mobilization of eosinophils by interleukin-5. Int Arch Allergy Immunol. 2005 Mar;136(3):295-302. Epub 2005 Feb 16. RESULTS: Interleukin (IL)-5, IL-6, and tumor necrosis factor (TNF) induced an eosinophil shape change, whereas interferon (IFN)-gamma significantly inhibited the shape change. We further analyzed the IFN-gamma effect, showing that pretreatment with IFN-gamma strongly suppressed IL-5-induced eosinophil shape change, and cycloheximide (CHX) abrogated the suppression by IFN-gamma, suggesting that new protein synthesis is required for the inhibitory effect by this cytokine. |
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19116254 | Han JY, Miller SA, Wolfe TM, Pourhassan H, Jerome KR: Cell type-specific induction and inhibition of apoptosis by Herpes Simplex virus type 2 ICP10. J Virol. 2009 Mar;83(6):2765-9. Epub 2008 Dec 30. HSV-2 ICP10 gene expression is sufficient to induce apoptosis in Jurkat cells, while its expression protects epithelial HEp-2 cells from apoptosis triggered by cycloheximide and tumor necrosis factor alpha. |
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17613518 | McKay MM, Morrison DK: Caspase-dependent cleavage disrupts the ERK cascade scaffolding function of KSR1. J Biol Chem. 2007 Sep 7;282(36):26225-34. Epub 2007 Jul 5. In addition, we find that in comparison with KSR1 (-/-) mouse embryonic fibroblasts expressing wild type KSR1 (WT-KSR1), cells expressing a cleavage-resistant KSR1 protein (DEVA-KSR1) exhibit reduced apoptotic signaling in response to tumor necrosis factor-alpha/cycloheximide treatment. |
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16040067 | Oguma K, Sano J, Kano R, Watari T, Hasegawa A: In vitro effect of recombinant human tumor necrosis factor-alpha on canine neutrophil apoptosis. Res Vet Sci. 2006 Apr;80(2):162-6. Epub 2005 Jul 22. However, PMN apoptosis was accelerated by rhTNF-alpha combined with cycloheximide. |
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17635918 | Jang BC, Sung SH, Park JG, Park JW, Bae JH, Shin DH, Park GY, Han SB, Suh SI: inhibits COX-2 by preventing COX-2 N-glycosylation and by increasing COX-2 protein turnover in a proteasome-dependent manner. J Biol Chem. 2007 Sep 21;282(38):27622-32. Epub 2007 Jul 16. GS-HCl (5 mM) was also able to decrease the molecular mass of endogenous and IL-1beta- or tumor necrosis factor-alpha-driven COX-2 in different human cell lines, including Hep2 (bronchial) and H292 (laryngeal). Remarkably, GS-HCl-mediated decrease in COX-2 molecular mass was associated with inhibition of COX-2 N-glycosylation during translation, as assessed by the effect of tunicamycin, the protein N-glycosylation inhibitor, or of cycloheximide, the translation inhibitor, on COX-2 modification. |
hydrochloride specifically 1(0,0,0,1) | Details |
15569826 | Furst R, Brueckl C, Kuebler WM, Zahler S, Krotz F, Gorlach A, Vollmar AM, Kiemer AK: Atrial natriuretic peptide induces mitogen-activated protein kinase phosphatase-1 in human endothelial cells via Rac1 and NAD (P) H oxidase/Nox2-activation. Circ Res. 2005 Jan 7;96(1):43-53. Epub 2004 Nov 29. The cardiovascular hormone atrial natriuretic peptide (ANP) exerts anti-inflammatory effects on tumor necrosis factor-alpha-activated endothelial cells by inducing mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1). |
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16150474 | Yedowitz JC, Blaho JA: Herpes simplex virus 2 modulates apoptosis and stimulates NF-kappaB nuclear translocation during infection in human epithelial HEp-2 cells. Virology. 2005 Nov 25;342(2):297-310. Epub 2005 Sep 15. This finding is different from that observed previously with HSV-1. (iv) Infected cell factors produced during the HSV-2 (G) prevention window inhibited apoptosis induced by external TNFalpha plus cycloheximide treatment. (v) NF-kappaB translocated to nuclei and its presence in nuclei correlated with apoptosis prevention during HSV-2 (G) infection. (vi) Finally, clinical HSV-2 isolates induced and prevented apoptosis in HEp-2 cells in a manner similar to that of laboratory strains. |
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17429344 | Lee HT, Kim M, Jan M, Penn RB, Emala CW: Renal tubule necrosis and apoptosis modulation by A1 receptor expression. Kidney Int. 2007 Jun;71(12):1249-61. Epub 2007 Apr 11. Receptor-overexpressing cells were protected against peroxide-induced necrosis and tumor necrosis factor-alpha/cycloheximide-induced apoptosis. |
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18336852 | Lin CC, Tseng HW, Hsieh HL, Lee CW, Wu CY, Cheng CY, Yang CM: Tumor necrosis factor-alpha induces MMP-9 expression via p42/p44 MAPK, JNK, and nuclear factor-kappaB in A549 cells. Toxicol Appl Pharmacol. 2008 Jun 15;229(3):386-98. Epub 2008 Feb 9. Moreover, pretreatment with actinomycin D and cycloheximide attenuated TNF-alpha-induced MMP-9 expression. |
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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. The A172 cells, by contrast, were susceptible only with cycloheximide, whereas U373MG cells were not susceptible to TRAIL. |
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15965903 | Stanic I, Facchini A, Borzi RM, Vitellozzi R, Stefanelli C, Goldring MB, Guarnieri C, Facchini A, Flamigni F: Polyamine depletion inhibits apoptosis following blocking of survival pathways in human chondrocytes stimulated by tumor necrosis factor-alpha. J Cell Physiol. 2006 Jan;206(1):138-46. The combined treatment of C-28/I2 chondrocytes with TNF and cycloheximide (CHX) resulted in a effector caspase activation and internucleosomal DNA fragmentation. |
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17671691 | Kamohara H, Takahashi M, Ishiko T, Ogawa M, Baba H: Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-alpha and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor. Int J Oncol. 2007 Sep;31(3):627-32. Actinomycin D suppressed and cycloheximide augmented CXCL-8 mRNA which was induced by TNF-alpha or not. |
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17484878 | Deng W, Shuyu E, Tsukahara R, Valentine WJ, Durgam G, Gududuru V, Balazs L, Manickam V, Arsura M, VanMiddlesworth L, Johnson LR, Parrill AL, Miller DD, Tigyi G: The lysophosphatidic acid type 2 receptor is required for protection against radiation-induced intestinal injury. Gastroenterology. 2007 May;132(5):1834-51. Epub 2007 Mar 24. RESULTS: OTP was more efficacious than LPA in reducing gamma irradiation-, camptothecin-, or tumor necrosis factor alpha/cycloheximide-induced apoptosis and caspase-3-8, and caspase-9 activity in the IEC-6 cell line. |
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18289527 | Ogura H, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Ectodomain shedding of TNF receptor 1 induced by protein synthesis inhibitors regulates TNF-alpha-mediated activation of NF-kappaB and caspase-8. Exp Cell Res. 2008 Apr 1;314(6):1406-14. Epub 2008 Feb 6. It has been established that the protein synthesis inhibitor cycloheximide (CHX) sensitizes many types of cells to tumor necrosis factor (TNF)-alpha-induced apoptosis, mainly due to its ability to block de novo synthesis of cellular FLICE-inhibitory protein (c-FLIP). |
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18719026 | Buzzelli MD, Nagarajan M, Radtka JF, Shumate ML, Navaratnarajah M, Lang CH, Cooney RN: Nuclear factor-kappaB mediates the inhibitory effects of tumor necrosis factor-alpha on growth hormone-inducible gene expression in liver. Endocrinology. 2008 Dec;149(12):6378-88. Epub 2008 Aug 21. Cycloheximide did not antagonize the inhibitory effects of TNF on GH-inducible IGF-I expression. |
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17938269 | Abayasiriwardana KS, Barbone D, Kim KU, Vivo C, Lee KK, Dansen TB, Hunt AE, Evan GI, Broaddus VC: Malignant mesothelioma cells are rapidly sensitized to TRAIL-induced apoptosis by low-dose anisomycin via Bim. Mol Cancer Ther. 2007 Oct;6(10):2766-76. Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) holds promise for the treatment of tumors; however, many tumors are resistant to TRAIL alone. We previously showed that resistant malignant mesothelioma cells are sensitized to TRAIL-induced apoptosis by diverse toxic insults including chemotherapy, irradiation, or protein translation inhibitors such as cycloheximide. |
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