| Name | caspase 3 |
|---|---|
| Synonyms | Apopain; CASP 3; CASP3; CPP 32; CPP32; CPP32B; Caspase 3; Caspase 3 precursor… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. One involves a direct activation of caspase-3 by large amounts of caspase-8 generated at the DISC (Type I cells). |
2(0,0,0,2) | Details |
| 18157742 | Desharnais P, Dupere-Minier G, Hamelin C, Devine P, Bernier J: Involvement of CD45 in DNA fragmentation in apoptosis induced by mitochondrial perturbing agents. Apoptosis. 2008 Feb;13(2):197-212. In contrast to wild type CD45-positive T cells, the CD45-deficient T cell lines are resistant to the induction of DNA fragmentation and chromatin condensation following tributyltin (TBT) or H2O2 exposure, but not to cycloheximide-induced apoptosis. Subcellular partitioning showed a decrease in nuclear localisation of caspase-3 and DFF40. |
2(0,0,0,2) | Details |
| 15546873 | Liu XM, Peyton KJ, Ensenat D, Wang H, Schafer AI, Alam J, Durante W: Endoplasmic reticulum stress stimulates heme oxygenase-1 gene expression in vascular smooth muscle. J Biol Chem. 2005 Jan 14;280(2):872-7. Epub 2004 Nov 16. The induction of HO-1 by ER stress was blocked by actinomycin D or cycloheximide and was independent of any changes in HO-1 mRNA stability. Interestingly, ER stress stimulated SMC apoptosis, as demonstrated by annexin V binding, caspase-3 activation, and DNA laddering. |
1(0,0,0,1) | Details |
| 16158257 | Martinet W, De Meyer GR, Herman AG, Kockx MM: Amino acid deprivation induces both apoptosis and autophagy in murine C2C12 muscle cells. Biotechnol Lett. 2005 Aug;27(16):1157-63. In the present study, mouse C2C12 muscle cells were starved in Earle's Balanced Salt Solution or treated with TNF-alpha and cycloheximide to induce autophagy and apoptosis, respectively. However, some cells showed features of apoptosis including caspase-3 cleavage, chromatin condensation, DNA fragmentation and annexin V labeling. |
2(0,0,0,2) | Details |
| 15685617 | Suy S, Mitchell JB, Samuni A, Mueller S, Kasid U: tempo, a small molecule, induces apoptosis in prostate carcinoma cells and suppresses tumor growth in athymic mice. Cancer. 2005 Mar 15;103(6):1302-13. Tempo-induced loss of cell viability was blocked partially or completely after pretreatment of cells with actinomycin-D or cycloheximide, suggesting a de novo macromolecule synthesis-dependent mechanism of cell death. Enzymatic assays were performed to measure the activities of 2 proteases, i.e., caspase-9 and caspase-3, in tempo-treated cells. |
2(0,0,0,2) | Details |
| 18511708 | Wilson SM, Barbone D, Yang TM, Jablons DM, Bueno R, Sugarbaker DJ, Nishimura SL, Gordon GJ, Broaddus VC: mTOR mediates survival signals in malignant mesothelioma grown as tumor fragment spheroids. Am J Respir Cell Mol Biol. 2008 Nov;39(5):576-83. Epub 2008 May 29. Freshly resected mesothelioma tissue from 15 different patients was grown in vitro as 1- to 2-mm-diameter fragments, exposed to apoptotic agents for 48 hours with or without PI3K/Akt/mTOR inhibitors, and doubly stained for cytokeratin and cleaved caspase 3 to identify apoptotic mesothelioma cells. |
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. Also, caspase-3 activation was suppressed in the VEGF-D expressing MDA-MB-231 clone. |
1(0,0,0,1) | 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. Decreasing either guanylyltransferase or methyltransferase resulted in caspase-3 activation and elevated terminal deoxynucleotidyltransferase-mediated - nick end labeling (TUNEL) staining characteristic of 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 |
| 19220581 | Wu Q, Shao H, Darwin ED, Li J, Li J, Yang B, Webster KA, Yu H: Extracellular calcium increases CXCR4 expression on bone marrow-derived cells and enhances pro-angiogenesis therapy. J Cell Mol Med. 2009 Sep;13(9B):3764-73. Epub 2009 Feb 9. BMC subpopulations expressing VEGFR2 (+), CD34 (+) and cKit (+)/Sca-1 (+) were especially sensitive to The effects were blocked by influx inhibitors, anti-CaR antibody and the protein synthesis inhibitor cycloheximide, but not by the CXCR4 antagonist AMD3100. |
1(0,0,0,1) | Details |
| 15578516 | Marienfeld C, Yamagiwa Y, Ueno Y, Chiasson V, Brooks L, Meng F, Patel T: Translational regulation of XIAP expression and cell survival during hypoxia in human cholangiocarcinoma. Gastroenterology. 2004 Dec;127(6):1787-97. Reduction in eIF-4E expression by siRNA decreased tumor cell resistance to hypoxia, increased caspase-3 activation and apoptosis, and decreased cell survival compared with controls. Translational processes were deregulated by cycloheximide or rapamycin or by targeted deletion of eukaryotic initiation factor (eIF)-4E, a rate-limiting translational initiation factor using small interfering RNA (siRNA). |
1(0,0,0,1) | Details |
| 19453217 | Vinken M, Decrock E, De Vuyst E, Leybaert L, Vanhaecke T, Rogiers V: Biochemical characterisation of an in vitro model of hepatocellular apoptotic cell death. Altern Lab Anim. 2009 Apr;37(2):209-18. This study was set up to critically evaluate a commonly-used in vitro model of hepatocellular apoptotic cell death, in which freshly isolated hepatocytes, cultured in a monolayer configuration, are exposed to a combination of Fas ligand and cycloheximide for six hours. A set of well-acknowledged cell death markers was addressed: a) cell morphology was studied by light microscopy; b) apoptotic and necrotic cell populations were quantified by in situ staining with Annexin-V, Hoechst 33342 and propidium iodide (PI); c) apoptotic and necrotic activities were monitored by probing caspase 3-like activity and measuring the extracellular leakage of lactate dehydrogenase (LDH), respectively; and d) the expression of apoptosis regulators was investigated by immunoblotting. |
2(0,0,0,2) | Details |
| 18819247 | Bosio E, Seveso M, Dedja A, Luca G, Calvitti M, Calafiore R, Rigotti P, Busetto R, Ancona E, Cozzi E: protoporpyhrin reduces caspase-3,-7 enzyme activity in neonatal porcine islets, but does not inhibit cell death induced by TNF-alpha. Cell Transplant. 2008;17(6):587-98. In in vitro assessments of NPICC apoptosis, NPICC showed a high sensitivity to apoptotic stimulation using a combination of TNF-alpha and cycloheximide. Stimulation with TNF-alpha alone was sufficient to induce reproducible apoptotic responses as demonstrated by caspase-3,-7 activation and subdiploid DNA analysis. |
2(0,0,0,2) | Details |
| 19112105 | Kadohara K, Nagumo M, Asami S, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Caspase-8 mediates mitochondrial release of pro-apoptotic proteins in a manner independent of its proteolytic activity in apoptosis induced by the protein synthesis inhibitor acetoxycycloheximide in human leukemia Jurkat cells. J Biol Chem. 2009 Feb 27;284(9):5478-87. Epub 2008 Dec 26. Unlike caspase-3, -6, -7, and -9, a small but significant portion of caspase-8 was found to localize in mitochondria before and after exposure to Ac-CHX. |
1(0,0,0,1) | Details |
| 16786197 | Li Z, Zong H, Kong X, Zhang S, Wang H, Sun Q, Gu J: Cell surface beta 1, 4-galactosyltransferase 1 promotes apoptosis by inhibiting epidermal growth factor receptor pathway. Mol Cell Biochem. 2006 Oct;291(1-2):69-76. Epub 2006 Jun 20. Our previous studies have shown that overexpression of beta1,4-galactosyltransferase1 (beta1,4GT1) leads to increased apoptosis induced by cycloheximide (CHX) in SMMC-7721 human hepatocarcinoma cells. As a result, the release of cytochrome c from mitochondria to cytosol was increased and caspase-3 was activated. |
1(0,0,0,1) | Details |
| 19647171 | Chen DL, Zhou D, Chu W, Herrbrich PE, Jones LA, Rothfuss JM, Engle JT, Geraci M, Welch MJ, Mach RH: Comparison of radiolabeled isatin analogs for imaging apoptosis with positron emission tomography. Nucl Med Biol. 2009 Aug;36(6):651-8. We compared the ability of two novel radiolabeled isatins, [18F] WC-IV-3 and [11C] WC-98, to detect caspase-3 activation in a rat model of cycloheximide-induced liver injury. |
86(1,1,1,6) | Details |
| 15924153 | Jeon YK, Kim H, Park SO, Choi HY, Kim YA, Park SS, Kim JE, Kim YN, Kim CW: Resistance to Fas-mediated apoptosis is restored by cycloheximide through the downregulation of cellular FLIPL in NK/T-cell lymphoma. Lab Invest. 2005 Jul;85(7):874-84. Fas stimulation of Hank-1 and NK-YS cells showed little processing of caspase 8, caspase 3, or bid, although the proximal signaling molecules of the death-inducing signaling complex, namely, Fas, Fas-associated protein with a death domain, caspase 8, and bid were present in these cells. |
2(0,0,0,2) | Details |
| 15905291 | Eley A, Hosseinzadeh S, Hakimi H, Geary I, Pacey AA: Apoptosis of ejaculated human sperm is induced by co-incubation with Chlamydia trachomatis lipopolysaccharide. Hum Reprod. 2005 Sep;20(9):2601-7. Epub 2005 May 19. Caspase activity was also investigated by fluorimetry and by use of a pan-caspase inhibitor and caspase-3 inhibitor. |
2(0,0,0,2) | Details |
| 18466319 | Santa-Catalina MO, Garcia-Marin LJ, Bragado MJ: Lovastatin effect in rat neuroblasts of the CNS: inhibition of cap-dependent translation. J Neurochem. 2008 Aug;106(3):1078-91. Epub 2008 May 3. Cycloheximide treatment, which blocked protein synthesis, does not induce neuroblasts apoptosis. Concomitantly, lovastatin causes a decrease in eIF4G cellular amount, which is partially mediated by caspase (s) activity excluding caspase 3. |
1(0,0,0,1) | Details |
| 15863130 | Hougardy BM, van der Zee AG, van den Heuvel FA, Timmer T, de Vries EG, de Jong S: Sensitivity to Fas-mediated apoptosis in high-risk HPV-positive human cervical cancer cells: relationship with Fas, caspase-8, and Bid. Gynecol Oncol. 2005 May;97(2):353-64. Analysis of the Fas apoptotic pathway showed that anti-Fas treatment induced caspase-8 activation and concomitantly Bid cleavage, caspase-9 and caspase-3 activation, PARP cleavage and apoptosis in HeLa and CaSki. |
1(0,0,0,1) | 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. |
83(1,1,1,3) | Details |
| 17295206 | Uchiyama S, Yamaguchi M: and zinc synergistically stimulate apoptotic cell death and suppress RANKL signaling-related gene expression in osteoclastic cells. J Cell Biochem. 2007 Jun 1;101(3):529-42. plus zinc-induced increase in caspase-3 mRNA expression was completely inhibited in the presence of cycloheximide (10 (-7) M), an inhibitor of protein synthesis, or 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB; 10 (-6) M), an inhibitor of transcription activity. |
83(1,1,1,3) | Details |
| 15689959 | Aoyama K, Burns DM, Suh SW, Garnier P, Matsumori Y, Shiina H, Swanson RA: Acidosis causes endoplasmic reticulum stress and caspase-12-mediated astrocyte death. J Cereb Blood Flow Metab. 2005 Mar;25(3):358-70. Endoplasmic reticulum (ER) stress leads to activation of caspase-12, which in turn can lead to activation of caspase-3 and cell death. Cell death was reduced by the protein synthesis inhibitor cycloheximide, further suggesting an active cell death program. |
2(0,0,0,2) | Details |
| 16049355 | Hidajat R, Nagano-Fujii M, Deng L, Hotta H: Cleavage of the hepatitis C virus NS5A protein by caspase-3 in the interferon sensitivity-determining region in a sequence-dependent manner. Kobe J Med Sci. 2004;50(5-6):153-66. |
2(0,0,0,2) | 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. We demonstrated that epidermal growth factor (EGF) stimulation of fibroblast NR6WT expressing human EGF receptors blocks staurosporine-induced apoptosis by inhibiting the activation of caspase-3. 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. |
2(0,0,0,2) | Details |
| 17166486 | Takadera T, Ohyashiki T: Caspase-dependent apoptosis induced by calcineurin inhibitors was prevented by glycogen synthase kinase-3 inhibitors in cultured rat cortical cells. Brain Res. 2007 Feb 16;1133(1):20-6. Epub 2006 Dec 12. In addition, insulin growth factor-I (IGF-I) and cycloheximide completely blocked cell death. Moreover, caspase-3 activation was accompanied by calcineurin inhibitor-induced cell death. |
1(0,0,0,1) | Details |
| 18654850 | Greenspon J, Li R, Xiao L, Rao JN, Marasa BS, Strauch ED, Wang JY, Turner DJ: protects intestinal epithelial cells from apoptosis through the Akt signaling pathway. Dig Dis Sci. 2009 Mar;54(3):499-510. Epub 2008 Jul 25. This activation of Akt was associated with decreased levels of both caspase-3 protein levels and of caspase-3 activity. |
1(0,0,0,1) | Details |
| 18636177 | Yamaguchi M, Uchiyama S: Combination of and zinc has potent effects on apoptotic cell death and suppression of bone resorption-related gene expression in osteoclastic cells. Int J Mol Med. 2008 Aug;22(2):221-8. CRP plus zinc-induced increase in caspase-3 mRNA expression was completely inhibited in the presence of cycloheximide (10 (-7) M), an inhibitor of protein synthesis, or 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DBR; 10 (-6) M), an inhibitor of transcription activity. |
83(1,1,1,3) | Details |
| 15528219 | Kaur M, Agarwal C, Singh RP, Guan X, Dwivedi C, Agarwal R: Skin cancer chemopreventive agent, {alpha}-santalol, induces apoptotic death of human epidermoid carcinoma A431 cells via caspase activation together with dissipation of mitochondrial membrane potential and cytochrome c release. Carcinogenesis. 2005 Feb;26(2):369-80. Epub 2004 Nov 4. Pre-treatment of cells with caspase-8 or -9 inhibitor, pan caspase inhibitor or cycloheximide totally blocked alpha-santalol-caused caspase-3 activity and cleavage, but only partially reversed apoptotic cell death. |
82(1,1,1,2) | 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. The A172 cells, by contrast, were susceptible only with cycloheximide, whereas U373MG cells were not susceptible to TRAIL. They then evaluated DR5 expression and JNK, caspase 3, and caspase 7 activation by conducting immunoblot analyses. |
2(0,0,0,2) | Details |
| 16131831 | Lim SI, Kweon CH, Yang DK, Tark DS, Kweon JH: Apoptosis in Vero cells infected with Akabane, Aino and Chuzan virus. J Vet Sci. 2005 Sep;6(3):251-4. Although the treatment of cycloheximide blocked apoptosis in Vero cells infected with three viruses, actinomycin D did not prevent DNA oligomerization, thus indicating that de novo viral protein synthesis is critical for viral apoptosis. In addition, the activation of caspase-3 was also detected in Vero cells by indirect fluorescent assay. |
1(0,0,0,1) | Details |
| 18540098 | Kawauchi K, Tobiume K, Iwashita K, Inagaki H, Morikawa T, Shibukawa Y, Moriyama Y, Hirata H, Kamata H: Cycloprodigiosin hydrochloride activates the Ras-PI3K-Akt pathway and suppresses protein synthesis inhibition-induced apoptosis in PC12 cells. Biosci Biotechnol Biochem. 2008 Jun;72(6):1564-70. Epub 2008 Jun 7. In this study, we found a novel function of cPrG-HCl; to suppress cell death in PC12 cells, which is caused by protein synthesis inhibitors cycloheximide and actinomycin D. cPrG-HCl activated Akt and suppressed apoptosis, and this was accompanied by inhibition of caspase-3 activity and DNA fragmentation independently of its H (+)/Cl (-) symporter activity. |
81(1,1,1,1) | 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 |
| 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. Loss-of-function manipulations in the RVLM using anti-HSP60 antiserum or antisense hsp60 oligonucleotide exacerbated mortality by potentiating the cardiovascular depression during experimental endotoxaemia, alongside intensified nucleosomal DNA fragmentation, elevated cytoplasmic histone-associated DNA fragments or augmented cytochromec-caspase-3 cascade of apoptotic signalling in the RVLM. |
2(0,0,0,2) | Details |
| 16526045 | Hareramadas B, Rai U: Cellular mechanism of -induced thymic involution in wall lizard: caspase-dependent action. J Exp Zool A Comp Exp Biol. 2006 May 1;305(5):396-409. In the presence of TEC, a positive reaction for caspase-3, -7 and -9 and enzyme substrate, poly (ADP- polymerase (PARP) in response to E2 suggests the caspase-dependent thymocyte apoptosis in the wall lizard Hemidactylus flaviviridis. |
1(0,0,0,1) | Details |
| 18571430 | Gangadhar NM, Firestein SJ, Stockwell BR: A novel role for jun N-terminal kinase signaling in olfactory sensory neuronal death. Mol Cell Neurosci. 2008 Aug;38(4):518-25. Epub 2008 May 11. Here, we show that inhibition of transcription or translation, by actinomycin D or cycloheximide, respectively, suppresses pathways leading to death, prolonging the survival of OSNs in culture. We discovered that caspase activity and jun N-terminal kinase (JNK) signaling both play a role in OSN death, and inhibition of JNK activity suppresses effector caspase (caspase-3) activation. |
1(0,0,0,1) | Details |
| 16891117 | Zhou D, Chu W, Rothfuss J, Zeng C, Xu J, Jones L, Welch MJ, Mach RH: Synthesis, radiolabeling, and in vivo evaluation of an 18F-labeled isatin analog for imaging caspase-3 activation in apoptosis. Bioorg Med Chem Lett. 2006 Oct 1;16(19):5041-6. Epub 2006 Aug 7. Western blot analysis confirmed the presence of activated caspase-3 in the liver and spleen of cycloheximide-treated animals. |
35(0,1,1,5) | 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. |
33(0,1,1,3) | Details |
| 15808420 | Aronis A, Madar Z, Tirosh O: Mechanism underlying oxidative stress-mediated lipotoxicity: exposure of J774.2 macrophages to triacylglycerols facilitates mitochondrial reactive species production and cellular necrosis. Free Radic Biol Med. 2005 May 1;38(9):1221-30. TG induced elevated ROS levels and suppressed caspase-3 in apoptotic cells pretreated for 24 h with cycloheximide. |
32(0,1,1,2) | Details |
| 19454725 | Karahashi H, Michelsen KS, Arditi M: Lipopolysaccharide-induced apoptosis in transformed bovine brain endothelial cells and human dermal microvessel endothelial cells: the role of JNK. J Immunol. 2009 Jun 1;182(11):7280-6. Stimulation of transformed bovine brain endothelial cells (TBBEC) with LPS leads to apoptosis while human microvessel endothelial cells (HMEC) need the presence of cycloheximide (CHX) with LPS to induce apoptosis. LPS-induced apoptosis in TBBEC was hallmarked by the activation of caspase 3, caspase 6, and caspase 8 after the stimulation of LPS, followed by poly (ADP- polymerase cleavage and lactate dehydrogenase release. |
2(0,0,0,2) | Details |
| 15629159 | Li Z, Wang H, Zong H, Sun Q, Kong X, Jiang J, Gu J: Downregulation of beta1,4-galactosyltransferase 1 inhibits CDK11 (p58)-mediated apoptosis induced by cycloheximide. Biochem Biophys Res Commun. 2005 Feb 11;327(2):628-36. Knock down of beta1,4-GT 1 also inhibited the release of cytochrome c from mitochondria and caspase-3 processing. |
2(0,0,0,2) | Details |
| 16912191 | Ma Y, Yu WD, Kong RX, Trump DL, Johnson CS: Role of nongenomic activation of phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase/extracellular signal-regulated kinase 1/2 pathways in 1,25D3-mediated apoptosis in squamous cell carcinoma cells. Cancer Res. 2006 Aug 15;66(16):8131-8. These effects were nongenomic: they occurred rapidly and were not inhibited by cycloheximide or actinomycin D. In addition, siRNA-Akt transfection followed by 1,25D3 treatment induced apoptosis much sooner than 1,25D3 alone. siRNA-Akt and 1,25D3 induced caspase-10 activation, suppressed the expression of c-IAP1 and XIAP, and promoted 1,25D3-induced caspase-3 activation. |
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. Specific caspase inhibitors revealed that caspase-3, caspase-6, caspase-8, and caspase-9 were primarily involved in apoptosis induction. |
1(0,0,0,1) | Details |
| 19690070 | Behera MA, Dai Q, Garde R, Saner C, Jungheim E, Price TM: stimulates mitochondrial activity with subsequent inhibition of apoptosis in MCF-10A benign breast epithelial cells. Am J Physiol Endocrinol Metab. 2009 Aug 18. The reaction was inhibited by a specific progesterone receptor antagonist and not affected by the translation inhibitor, cycloheximide. treatment inhibited apoptosis induced by activation of the FasL pathway, as shown by a decrease in sub-G1 cell fraction during fluorescence-activated cell sorting and a decrease in caspase 3/7 levels. |
1(0,0,0,1) | Details |
| 17352013 | Ustundag Y, Bronk SF, Gores GJ: Proteasome inhibition-induces endoplasmic reticulum dysfunction and cell death of human cholangiocarcinoma cells. World J Gastroenterol. 2007 Feb 14;13(6):851-7. The protein synthesis inhibitor, cycloheximide, blocked apoptosis induced by proteasome inhibitor indicating that ER dysfunction was dependent upon the formation of new proteins. Caspase 3/7 activity was assessed using an enzymatic-based fluorescent assay. |
1(0,0,0,1) | Details |
| 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. |
32(0,1,1,2) | Details |
| 17283163 | Little JL, Wheeler FB, Fels DR, Koumenis C, Kridel SJ: Inhibition of fatty acid synthase induces endoplasmic reticulum stress in tumor cells. Cancer Res. 2007 Feb 1;67(3):1262-9. FAS inhibitor-induced ER stress is activated prior to the detection of caspase 3 and PARP cleavage, primary indicators of cell death, whereas orlistat-induced cell death is rescued by coincubation with the global translation inhibitor cycloheximide. |
31(0,1,1,1) | Details |
| 20005201 | Sengupta R, Billiar TR, Kagan VE, Stoyanovsky DA: and thioredoxin type 1 modulate the activity of caspase 8 in HepG2 cells. Biochem Biophys Res Commun. 2010 Jan 1;391(1):1127-30. Epub 2009 Dec 11. The data obtained suggest that extrinsic apoptosis can be subjected to redox regulation before induction of proteolytic damage by caspase 3. |
1(0,0,0,1) | Details |
| 16585560 | Yoshioka Y, Kitao T, Kishino T, Yamamuro A, Maeda S: protects macrophages from peroxide-induced apoptosis by inducing the formation of catalase. J Immunol. 2006 Apr 15;176(8):4675-81. H2O2-treated cells showed apoptotic features, such as activation of caspase-9 and caspase-3, nuclear fragmentation, and DNA fragmentation. Cycloheximide, a protein synthesis inhibitor, inhibited both the NO-induced increase in the catalase level and the cytoprotective effect of NO. |
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). Apoptosis was followed by measuring changes in nuclear morphology, caspase-3 activity, poly-ADP- polymerase cleavage or punctation of mRFP-Bax on mitochondria. |
1(0,0,0,1) | 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. Lastly, all ROS inhibitors inhibited caspase-3 activity. |
1(0,0,0,1) | 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. |
31(0,1,1,1) | 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. 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. |
31(0,1,1,1) | Details |
| 19384564 | Smith AJ, Smith RA, Stone TW: 5-Hydroxyanthranilic acid, a metabolite, generates oxidative stress and neuronal death via p38 activation in cultured cerebellar granule neurones. Neurotox Res. 2009 May;15(4):303-10. Epub 2009 Mar 4. The results indicate that metabolites can be via a caspase-3 independent mechanism, and that the minor metabolite 5HAA is as potent a toxin as the better documented compounds 3HK and 3HAA. |
1(0,0,0,1) | Details |
| 16325375 | Zhang L, Tie Y, Tian C, Xing G, Song Y, Zhu Y, Sun Z, He F: CKIP-1 recruits nuclear ATM partially to the plasma membrane through interaction with ATM. Cell Signal. 2006 Sep;18(9):1386-95. Epub 2005 Dec 1. More recently, we showed that CKIP-1 regulated AP-1 activity and promoted apoptosis via caspase-3-dependent cleavage and translocation. Here, we report that overexpression of CKIP-1 in SK-BR-3 breast cancer cells prevents p53 degradation induced by cycloheximide treatment through increase of p53 N-terminal Ser-15 phosphorylation level. |
1(0,0,0,1) | Details |
| 15685448 | Tahara E Jr, Tahara H, Kanno M, Naka K, Takeda Y, Matsuzaki T, Yamazaki R, Ishihara H, Yasui W, Barrett JC, Ide T, Tahara E: G1P3, an interferon inducible gene 6-16, is expressed in gastric cancers and inhibits mitochondrial-mediated apoptosis in gastric cancer cell line TMK-1 cell. Cancer Immunol Immunother. 2005 Aug;54(8):729-40. Epub 2005 Feb 1. One of exceptional gastric cancer cell line, TMK-1, which do not express detectable 6-16, is sensitive to apoptosis induced by cycloheximide (CHX), 5-fluorouracil (5-FU) and serum-deprivation. Ectopic expression of 6-16 gene restored the induction of apoptosis and inhibited caspase-3 activity in TMK-1 cells. |
1(0,0,0,1) | Details |
| 16734383 | Dunford JE, Rogers MJ, Ebetino FH, Phipps RJ, Coxon FP: Inhibition of protein prenylation by bisphosphonates causes sustained activation of Rac, Cdc42, and Rho GTPases. J Bone Miner Res. 2006 May;21(5):684-94. The Rac-GTP that increased after N-BP treatment was newly translated, cytoplasmic unprenylated protein, because it was not labeled with [(14) C] and the increase in Rac-GTP was prevented by cycloheximide. The effect of N-BPs, or decreasing Rac expression using siRNA, on downstream p38 activity was evaluated by Western blotting and apoptosis assessed by measurement of caspase 3/7 activity. |
1(0,0,0,1) | 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. Pretreatment with cycloheximide showed that active caspase-3 fragments have a high turnover rate in OVCAR3 R350 cells. |
11(0,0,1,6) | 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. However when apoptosis was stimulated with cycloheximide, the schizophrenia group showed an attenuated caspase-3 response. |
8(0,0,1,3) | Details |
| 18251703 | Liang M, Russell G, Hulley PA: Bim, Bak, and Bax regulate osteoblast survival. J Bone Miner Res. 2008 May;23(5):610-20. Detailed analysis of the mouse line showed that both mRNA and protein levels rose from 2 h to peak between 16 and 24 h, in conjunction with activation of caspase 3 and rising levels of apoptosis. Both actinomycin D and cycloheximide prevented this increase in Bim, indicating transcriptional regulation. |
1(0,0,0,1) | Details |
| 18360057 | Hayashi H, Kobara M, Abe M, Tanaka N, Gouda E, Toba H, Yamada H, Tatsumi T, Nakata T, Matsubara H: nongenomically produces oxidase-dependent reactive species and induces myocyte apoptosis. Hypertens Res. 2008 Feb;31(2):363-75. Neither an inhibitor for nuclear transcription (actinomycin D) nor an inhibitor of new protein synthesis (cycloheximide) blocked this rapid activation, and specific binding of to plasma membrane fraction was inhibited by eplerenone, suggesting a nongenomic mechanism. Nuclear staining with DAPI showed that (10 (-7) mol/L) increased the myocyte apoptosis (2.3 fold, p <0.001), coincident with the activation of caspase-3 (1.4 fold, p <0.05), compared with the serum-deprived control after 48 h. |
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 |
| 16596277 | Nakatani H, Araki K, Jin T, Kobayashi M, Sugimoto T, Akimori T, Namikawa T, Okamoto K, Nakano T, Okabayashi T, Hokimoto N, Kitagawa H, Taguchi T: STI571 (Glivec) induces cell death in the gastrointestinal stromal tumor cell line, GIST-T1, via endoplasmic reticulum stress response. Int J Mol Med. 2006 May;17(5):893-7. In these cells, STI571 induced pro-caspase-12 or pro-caspase-7 cleavage and it affected caspase-3 activity and induced the endoplasmic reticulum (ER)-resident chaperone, -regulated protein 78. The STI571-induced cell death was blocked by the protein synthesis inhibitor, cycloheximide. |
1(0,0,0,1) | Details |
| 19671668 | Huang SK, White ES, Wettlaufer SH, Grifka H, Hogaboam CM, Thannickal VJ, Horowitz JC, Peters-Golden M: (2) induces fibroblast apoptosis by modulating multiple survival pathways. FASEB J. 2009 Dec;23(12):4317-26. Epub 2009 Aug 11. As compared to medium alone, 24 h of treatment with PGE (2) increased apoptosis of normal lung fibroblasts in a dose-dependent manner (EC (50) approximately 50 nM), as measured by annexin V staining, caspase 3 activity, cleavage of poly-ADP- polymerase, and single-stranded DNA levels. PGE (2) also potentiated apoptosis elicited by Fas ligand plus cycloheximide. |
1(0,0,0,1) | Details |
| 18474237 | Lee JM, Kim YJ, Ra H, Kang SJ, Han S, Koh JY, Kim YH: The involvement of caspase-11 in TPEN-induced apoptosis. FEBS Lett. 2008 Jun 11;582(13):1871-6. Epub 2008 May 12. Caspase-11 activity also increased, which resulted in caspase-3 activation. Cycloheximide or actinomycin D blocked caspase-11 induction, reduced caspase-11 and -3 activation, and attenuated TPEN-induced neuronal apoptosis. |
1(0,0,0,1) | Details |
| 16787641 | Ito Y, Oh-Hashi K, Kiuchi K, Hirata Y: p44/42 MAP kinase and c-Jun N-terminal kinase contribute to the up-regulation of caspase-3 in -induced apoptosis in PC12 cells. Brain Res. 2006 Jul 12;1099(1):1-7. Epub 2006 Jun 19. Up-regulation of caspase-3 protein was evident in -treated PC12 cells and was moderate in cisplatin-, rotenone- and A23187-treated cells but was not observed in serum deprivation-, anisomycin-, camptothecin-, cycloheximide- or staurosporine-treated cells in which all treatments induced extensive DNA fragmentation. |
7(0,0,0,7) | Details |
| 19559790 | Shioiri T, Muroi M, Hatao F, Nishida M, Ogawa T, Mimura Y, Seto Y, Kaminishi M, Tanamoto K: Caspase-3 is activated and rapidly released from human umbilical vein endothelial cells in response to lipopolysaccharide. Biochim Biophys Acta. 2009 Oct;1792(10):1011-8. Epub 2009 Jun 25. In the presence of cycloheximide (CHX), an increase in intracellular caspase-3/7 activity in response to LPS was not detected in HUVEC up to 24 h following stimulation even in the presence of LPS-binding protein (LBP), soluble CD14 and soluble MD-2, whereas the decrease in cell viability and increase in release of the cellular enzyme lactate dehydrogenase (LDH) were observed in a soluble CD14/LBP-dependent manner. |
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| 16116236 | Krishnan S, Kiang JG, Fisher CU, Nambiar MP, Nguyen HT, Kyttaris VC, Chowdhury B, Rus V, Tsokos GC: Increased caspase-3 expression and activity contribute to reduced CD3zeta expression in systemic lupus erythematosus T cells. J Immunol. 2005 Sep 1;175(5):3417-23. |
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| 16180102 | Jiang Y, Cheng DW, Crook ED, Singh LP: Transforming growth factor-beta1 regulation of laminin gamma1 and fibronectin expression and survival of mouse mesangial cells. Mol Cell Biochem. 2005 Oct;278(1-2):165-75. TGF-beta1 elevates pro-apoptotic caspase-3 activity and decrease cell cycle progression factor cyclin D1 expression, which parallels cell death. |
1(0,0,0,1) | Details |
| 15897232 | Sakao S, Taraseviciene-Stewart L, Lee JD, Wood K, Cool CD, Voelkel NF: Initial apoptosis is followed by increased proliferation of apoptosis-resistant endothelial cells. FASEB J. 2005 Jul;19(9):1178-80. Epub 2005 May 16. Immunohistochemical staining for caspase-3 and PCNA and flow cytometry for Annexin-V and BrdU supported our concept, since SU5416 caused initial apoptosis (35.8% at 24 h after the SU5416 addition and 4.8% in control cells) whereas the surviving cells became hyperproliferative (PCNA positive). |
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| 19117118 | Femenia F, Huet D, Lair-Fulleringer S, Wagner MC, Sarfati J, Shingarova L, Guillot J, Boireau P, Chermette R, Berkova N: Effects of conidia of various Aspergillus species on apoptosis of human pneumocytes and bronchial epithelial cells. Mycopathologia. 2009 May;167(5):249-62. Epub 2009 Jan 1. For TNF-induced apoptosis, the anti-apoptotic effect of conidia of all isolates was found to be associated with a reduction of caspase-3 in human cells. |
1(0,0,0,1) | Details |
| 15647476 | Verma P, Chierzi S, Codd AM, Campbell DS, Meyer RL, Holt CE, Fawcett JW: Axonal protein synthesis and degradation are necessary for efficient growth cone regeneration. J Neurosci. 2005 Jan 12;25(2):331-42. Application of protein synthesis inhibitors (cycloheximide and anisomycin) to cut axons, including axons whose cell bodies were removed, or proteasome inhibitors (lactacystin and N-acetyl-Nor---Al) all result in a reduction in the proportion of transected axons able to reform growth cones. Similar inhibition of growth cone formation was observed on addition of target of rapamycin (TOR), p38 MAPK (mitogen-activated protein kinase), and caspase-3 inhibitors. |
1(0,0,0,1) | Details |
| 17647100 | Takadera T, Ohyashiki T: Calmodulin inhibitor-induced apoptosis was prevented by glycogen synthase kinase-3 inhibitors in PC12 cells. Cell Mol Neurobiol. 2007 Sep;27(6):783-90. Epub 2007 Jul 24. In addition, nerve growth factor and cycloheximide, a protein synthesis inhibitor, completely blocked cell death. Moreover, caspase-3 activation was accompanied by calmodulin inhibitor-induced cell death and inhibited by nerve growth factor. |
1(0,0,0,1) | Details |
| 18192502 | Medler TR, Petrusca DN, Lee PJ, Hubbard WC, Berdyshev EV, Skirball J, Kamocki K, Schuchman E, Tuder RM, Petrache I: Apoptotic sphingolipid signaling by ceramides in lung endothelial cells. . Am J Respir Cell Mol Biol. 2008 Jun;38(6):639-46. Epub 2008 Jan 10. Intermediate-chain length (C (8:0)) extracellular ceramides, used as a surrogate of paracellular ceramides, triggered caspase-3 activation in primary mouse lung endothelial cells, similar to TNF-alpha-generated endogenous ceramides. Inhibitory siRNA against serine palmitoyl transferase subunit 1 but not acid sphingomyelinase inhibited both C (8:0) - and TNF-alpha (plus cycloheximide)-induced apoptosis, consistent with the requirement for activation of the de novo pathway of sphingolipid synthesis. |
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. Especially, AML1-ETO endows leukemic cells with the susceptibility to anti-Fas agonist antibody, ultraviolet light and camptothecin analog NSC606985-induced apoptosis with increased activation of caspase-3/8. |
1(0,0,0,1) | Details |
| 18300075 | Shih SR, Weng KF, Stollar V, Li ML: Viral protein synthesis is required for Enterovirus 71 to induce apoptosis in human glioblastoma cells. J Neurovirol. 2008 Jan;14(1):53-61. Apoptosis was inhibited when EV71-infected cells were treated with chloroquine, HCl, or cycloheximide. |
0(0,0,0,0) | Details |
| 17123514 | Theiss C, Mazur A, Meller K, Mannherz HG: Changes in gap junction organization and decreased coupling during induced apoptosis in lens epithelial and NIH-3T3 cells. Exp Cell Res. 2007 Jan 1;313(1):38-52. Epub 2006 Oct 13. We demonstrate that global induction of apoptosis in primary bovine lens epithelial (LEC) or fibroblastic mouse NIH-3T3 cells by staurosporine, puromycin, cycloheximide, or etoposide is accompanied by a decrease in coupling by gap junctions. Cell coupling as tested by neurobiotin spreading was maintained when the LEC or NIH-3T3 cells were pre-incubated with the pan-caspase inhibitor zVAD or the caspase-3 inhibiting tetrapeptide DEVD. |
3(0,0,0,3) | Details |
| 17121821 | Sunyach C, Cisse MA, da Costa CA, Vincent B, Checler F: The C-terminal products of cellular prion protein processing, C1 and C2, exert distinct influence on p53-dependent staurosporine-induced caspase-3 activation. J Biol Chem. 2007 Jan 19;282(3):1956-63. Epub 2006 Nov 22. |
3(0,0,0,3) | Details |
| 18474417 | Zanotto-Filho A, Cammarota M, Gelain DP, Oliveira RB, Delgado-Canedo A, Dalmolin RJ, Pasquali MA, Moreira JC: induces apoptosis by a non-classical mechanism of ERK1/2 activation. Toxicol In Vitro. 2008 Aug;22(5):1205-12. Epub 2008 Apr 7. In this work, we reported that RA treatment for 24 h decreases cell viability, induces apoptosis dependent on caspase-3 activation, and activates the transcription factor AP-1 in cultured Sertoli cells. ERK1/2 activation was mediated by MEK1/2, and the protein synthesis inhibitor cycloheximide did not alter the pattern of RA-induced ERK1/2 phosphorylation. |
3(0,0,0,3) | Details |
| 17045392 | Iga M, Iwami M, Sakurai S: Nongenomic action of an insect steroid hormone in steroid-induced programmed cell death. Mol Cell Endocrinol. 2007 Jan 15;263(1-2):18-28. Epub 2006 Oct 11. A protein synthesis inhibitor, cycloheximide (CHX, 2 mM) induced a cell death that exhibited only nuclear and DNA fragmentation. In addition, we show a possible involvement of Ca2+-PKC-caspase-3 like protease pathway in the nongenomic action. |
1(0,0,0,1) | Details |
| 15876423 | Chow JM, Shen SC, Huan SK, Lin HY, Chen YC: but not rutin and quercitrin, prevention of H2O2-induced apoptosis via anti-oxidant activity and heme oxygenase 1 gene expression in macrophages. Biochem Pharmacol. 2005 Jun 15;69(12):1839-51. Results of Western blotting show that QE but not its glycoside rutin (RUT) and quicitrin-induced HO-1 protein expression in a time- and dose-dependent manner, and HO-1 protein induced by QE was blocked by an addition of cycloheximide or actinomycin D. |
0(0,0,0,0) | Details |
| 16647178 | Chen TJ, Jeng JY, Lin CW, Wu CY, Chen YC: inhibition of ROS-dependent and -independent apoptosis in rat glioma C6 cells. Toxicology. 2006 Jun 1;223(1-2):113-26. Epub 2006 Mar 22. Induction of HO-1 protein expression was detected in QUE- but not RUT- or QUI-treated C6 cells, and this was prevented by cycloheximide and actinomycin D. |
0(0,0,0,0) | 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. Bile salts inhibited formation of the active caspase-3 from its precursor procaspase-3. |
3(0,0,0,3) | Details |
| 16427675 | Chen D, Texada DE, Duggan C, Deng Y, Redens TB, Langford MP: Caspase-3 and -7 mediate apoptosis of human Chang's conjunctival cells induced by enterovirus 70. Virology. 2006 Apr 10;347(2):307-22. Epub 2006 Jan 20. EV70-induced apoptosis was inhibited by cycloheximide and methoxysuccinyl---Pro-Val-chloromethylketone (MPCMK), but not actinomycin D and guanidine.HCl (although guanidine.HCl inhibited the apoptosis induced by EV70 infection at 0.5 PFU/cell for 18 h). |
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| 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. Cisplatin-induced loss of Mcl-1 occurs at the same time as the mitochondrial release of cytochrome c, activation of caspase-3, and initiation of apoptosis. Treatment of cells with cycloheximide, a protein synthesis inhibitor, revealed rapid turnover of Mcl-1. |
3(0,0,0,3) | 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. |
3(0,0,0,3) | Details |
| 16215688 | Singh S, Khar A: Differential gene expression during apoptosis induced by a serum factor: role of mitochondrial F0-F1 ATP synthase complex. Apoptosis. 2005 Dec;10(6):1469-82. Caspase 1 and caspase 3 activity and the loss of mitochondrial membrane potential were also inhibited by oligomycin during apoptosis in these cells, suggesting that the oligomycin induced inhibition of apoptosis could be due to inhibition of caspase activity and inhibition of mitochondrial depolarization. |
1(0,0,0,1) | 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. produced extensive Bax-dependent caspase-3 activation and neuron apoptosis in the cerebellar internal granule cell layer, which was maximal at approximately 6 hours postadministration. |
1(0,0,0,1) | Details |
| 17532486 | Lin HY, Shen SC, Lin CW, Yang LY, Chen YC: Baicalein inhibition of peroxide-induced apoptosis via ROS-dependent heme oxygenase 1 gene expression. Biochim Biophys Acta. 2007 Jul;1773(7):1073-86. Epub 2007 Apr 22. In the present study, baicalein (BE) but not its glycoside, baicalin (BI), induced heme oxygenase-1 (HO-1) gene expression at both the mRNA and protein levels, and the BE-induced HO-1 protein was blocked by adding cycloheximide (CHX) or actinomycin D (Act D). |
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 |
| 17879164 | Shaltouki A, Freer M, Mei Y, Weyman CM: Increased expression of the pro-apoptotic Bcl2 family member PUMA is required for mitochondrial release of cytochrome C and the apoptosis associated with skeletal myoblast differentiation. Apoptosis. 2007 Dec;12(12):2143-54. We have previously shown that when skeletal myoblasts are cultured in differentiation medium (DM), roughly 30% undergo caspase 3-dependent apoptosis rather than differentiation. Inclusion of cycloheximide inhibits the release of cytochrome C, the activation of caspase 9 and apoptosis. |
3(0,0,0,3) | 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. FIZZ1 treatment also inhibited the apoptotic agent-induced activities of caspase-3 and caspase-8. |
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| 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. PQ induced morphological and biochemical features that were consistent with apoptosis, including dose-dependent cytochrome c release, with subsequent caspase-3 and poly (ADP- polymerase cleavage. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. |
1(0,0,0,1) | Details |
| 15542778 | Doi S, Soda H, Oka M, Tsurutani J, Kitazaki T, Nakamura Y, Fukuda M, Yamada Y, Kamihira S, Kohno S: The histone deacetylase inhibitor FR901228 induces caspase-dependent apoptosis via the mitochondrial pathway in small cell lung cancer cells. Mol Cancer Ther. 2004 Nov;3(11):1397-402. In addition, the combination of bcl-2 antisense oligonucleotides with FR901228 enhanced FR901228-induced caspase-3 activity and cytotoxicity. |
1(0,0,0,1) | Details |
| 16330215 | Fujimoto S, Katsuki H, Kume T, Akaike A: Thrombin-induced delayed injury involves multiple and distinct signaling pathways in the cerebral cortex and the striatum in organotypic slice cultures. Neurobiol Dis. 2006 Apr;22(1):130-42. Epub 2005 Dec 5. These effects were prevented by cycloheximide and actinomycin D but not by a caspase-3 inhibitor. |
0(0,0,0,0) | Details |
| 19331698 | Wegrzyn P, Yarwood SJ, Fiegler N, Bzowska M, Koj A, Mizgalska D, Malicki S, Pajak M, Kasza A, Kachamakova-Trojanowska N, Bereta J, Jura J, Jura J: Mimitin - a novel cytokine-regulated mitochondrial protein. BMC Cell Biol. 2009 Mar 31;10:23. However, when apoptosis was induced by TNF and cycloheximide, and mimitin expression blocked, the activities of these caspases were significantly increased. |
0(0,0,0,0) | Details |
| 16330024 | Fish RJ, Kruithof EK: Evidence for serpinB2-independent protection from TNF-alpha-induced apoptosis. Exp Cell Res. 2006 Feb 1;312(3):350-61. Epub 2005 Dec 5. Stimulation with TNF-alpha protected each cell type from apoptosis induced by TNF-alpha and cycloheximide. |
0(0,0,0,0) | Details |
| 17628625 | Sumi D, Manji A, Shinkai Y, Toyama T, Kumagai Y: Activation of the Nrf2 pathway, but decreased gamma-glutamylcysteine synthetase heavy subunit chain levels and caspase-3-dependent apoptosis during exposure of primary mouse hepatocytes to diphenylarsinic acid. Toxicol Appl Pharmacol. 2007 Sep 15;223(3):218-24. Epub 2007 Jun 18. Experiments with cycloheximide revealed that the DPAsV-mediated reduction in gamma-GCS (H) was due to a post-translational modification. |
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| 20032379 | Eriksson D, Lofroth PO, Johansson L, Riklund K, Stigbrand T: Apoptotic signalling in HeLa Hep2 cells following 5 Gy of -60 gamma radiation. Anticancer Res. 2009 Nov;29(11):4361-6. The activation of caspase-2, caspase-8, caspase-9 and effector caspase-3 was investigated by caspase assay plates and Western blots. HeLa Hep2 cells were irradiated with or without preincubation with inhibitors of protein synthesis (cycloheximide, CHX) and caspases, followed by TUNEL staining and caspase assay plate evaluation. |
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| 15537749 | Johnson VJ, Kim SH, Sharma RP: Aluminum-maltolate induces apoptosis and necrosis in neuro-2a cells: potential role for p53 signaling. Toxicol Sci. 2005 Feb;83(2):329-39. Epub 2004 Nov 10. Treatment with Al-malt resulted in caspase 3 activation and the externalization of phosphatidyl serine, both indicative of apoptosis. Interestingly, pretreatment with cycloheximide (CHX), a potent protein synthesis inhibitor markedly reduced Al-malt-induced apoptosis, indicating that altered gene expression was critical for this form of cell death. |
1(0,0,0,1) | Details |
| 17157182 | Pardo M, Melendez JA, Tirosh O: Manganese superoxide dismutase inactivation during Fas (CD95)-mediated apoptosis in Jurkat T cells. Free Radic Biol Med. 2006 Dec 15;41(12):1795-806. Epub 2006 Sep 16. In the presence of cycloheximide, an inhibitor of protein synthesis, the rates of cell death and MnSOD degradation were accelerated. Moreover, two possible cleavage sites of recombinant hMnSOD by direct interaction with recombinant caspase-3 were noted. |
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. 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 |