| Name | annexin V |
|---|---|
| Synonyms | ANX 5; PP4; ENX2; ANX5; ANXA 5; ANXA5; Anchorin CII; Annexin 5… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. DAPI assay, Annexin V and PI double staining, Western blot assay and immunoprecipitation were used to determine the effect of Compound K on the induction of apoptosis. |
2(0,0,0,2) | 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. |
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 |
| 17366325 | Hallock S, Tang SC, Buja LM, Trump BF, Liepins A, Weerasinghe P: Aurintricarboxylic acid inhibits protein synthesis independent, sanguinarine-induced apoptosis and oncosis. Toxicol Pathol. 2007;35(2):300-9. The pretreatment effects of both chemical compounds on apoptosis and oncosis-BCD were evaluated by measuring multiple parameters using quantitative morphology, electron microscopy, terminal deoxynucleotidyl transferase (TdT) end-labeling and annexin-V-binding. |
1(0,0,0,1) | 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. To examine whether the nongenomic activation of Akt and ERK1/2 plays a role in 1,25D3-mediated apoptosis, the expression of Akt or ERK1/2 was reduced by small interfering RNA (siRNA). siRNA-Akt significantly enhanced 1,25D3-induced apoptosis as indicated by increased levels of Annexin V-positive cells and increased sub-G (1) population and DNA fragmentation. |
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. |
1(0,0,0,1) | Details |
| 18199340 | Jiang Q, Wei H, Tian Z: Poly I:C enhances cycloheximide-induced apoptosis of tumor cells through TLR3 pathway. BMC Cancer. 2008 Jan 17;8:12. All tumor cell lines were cultured with poly I:C, CHX, or both for 12 h, 24 h, 72 h, and then the cell viability was analyzed with CellTiter 96 (R) AQueous One Solution, the apoptosis was measured by FACS with Annexin V and PI staining. |
1(0,0,0,1) | Details |
| 16778395 | Park WS, Sung DK, Kang S, Koo SH, Kim YJ, Lee JH, Chang YS, Lee M: Therapeutic window for cycloheximide treatment after hypoxic-ischemic brain injury in neonatal rats. J Korean Med Sci. 2006 Jun;21(3):490-4. Apoptosis or necrosis was identified by performing flow cytometry with a combination of fluorescinated annexin V and propidium iodide, and the extent of cerebral infarction was evaluated with triphenyl tetrazolium (TTC) at 48 hr and 72 hr after HI, respectively. |
1(0,0,0,1) | 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. METHODS: The apoptotic effects of tempo were examined by the flow cytometric analysis of cells labeled with fluorescein isothiocyanate-conjugated annexin-V, and by electron microscopy. |
1(0,0,0,1) | Details |
| 17147231 | Liang PY, Zeng YY, Wang T, Xing FY, Zhao JX, Jiang X, Di JF: [The effect of p38 on the cycloheximide-induced HL-60 cell death through mitochondria pathway]. Zhonghua Xue Ye Xue Za Zhi. 2006 Jun;27(6):398-402. Sub-diploid cell ratio was detected by PI staining flow cytometry at 6, 9, 12, 18, 24 h time points, and apoptotic cell ratio by Annexin V-FITC/PI double staining flow cytometry at 6 h and 18 h time points. |
1(0,0,0,1) | Details |
| 18547754 | Lee K, Hyslop JM, Nanassy L, Machaty Z: Incidence of apoptosis in parthenogenetic porcine embryos generated by using protein kinase or protein synthesis inhibitors. Anim Reprod Sci. 2009 Jun;112(3-4):261-72. Epub 2008 May 3. In the present research, we investigated whether I and cycloheximide, two chemicals frequently used in combined oocyte activation protocols, have any detrimental effect on programmed cell death in the developing porcine embryo. The annexin V assay revealed that flip (another early apoptotic event) took place in 24.4+/-2.1 to 32.3+/-2.4% of the blastomeres. |
1(0,0,0,1) | Details |
| 17575110 | Liu T, Hannafon B, Gill L, Kelly W, Benbrook D: Flex-Hets differentially induce apoptosis in cancer over normal cells by directly targeting mitochondria. Mol Cancer Ther. 2007 Jun;6(6):1814-22. Inhibition of protein synthesis with cycloheximide also did not prevent Flex-Het mitochondrial or apoptosis effects. Mitochondrial effects and apoptosis were measured using JC-1 and Annexin V-FITC dyes with flow cytometry. |
1(0,0,0,1) | Details |
| 18094537 | Ikewaki N, Tamauchi H, Inoko H: Decrease in CD93 (C1qRp) expression in a human monocyte-like cell line (U937) treated with various apoptosis-inducing chemical substances. Microbiol Immunol. 2007;51(12):1189-200. Apoptosis was monitored using two-color flow cytometry with Annexin V and 7-amino actinomycin D (7AAD). |
1(0,0,0,1) | Details |
| 17097791 | Lock EA, Reed CJ, Kinsey GR, Schnellmann RG: Caspase-dependent and -independent induction of externalization during apoptosis in human renal carcinoma Cak (1)-1 and A-498 cells. Toxicology. 2007 Jan 5;229(1-2):79-90. Epub 2006 Oct 13. Subsequent experiments were conducted to determine mediators of externalization, using annexin V binding, when caspases were inhibited. The endonuclease inhibitor aurintricarboxylic acid (ATA), phospholipase A (2) inhibitor bromoenol lactone (BEL), protein synthesis inhibitor cycloheximide (CH) and chloride channel blockers niflumic acid (NFA) and 5-nitro-2-(3-phenylpropylamino) (NPPB) all had no effect on staurosporine-induced annexin V binding in A-498 cells either in the presence or absence of ZVAD. |
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). |
1(0,0,0,1) | Details |
| 16614525 | Park WS, Sung DK, Kang S, Koo SH, Kim YJ, Lee JH, Chang YS, Lee M: Neuroprotective effect of cycloheximide on hypoxic-ischemic brain injury in neonatal rats. J Korean Med Sci. 2006 Apr;21(2):337-41. Apoptosis was identified by performing terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) staining and flow cytometry with a combination of fluoresceinated annexin V and propidium iodide. |
1(0,0,0,1) | 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. Results were compared with several reference tests to measure apoptosis including DNA fragmentation, annexin V staining, and light microscopy. |
1(0,0,0,1) | 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. Cell apoptosis was assessed by human annexin V binding, and caspase 8 activation was assessed by flow cytometry. |
1(0,0,0,1) | 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. Fluorescence-activated cell sorting analysis of Annexin V/propidium iodide (PI) stained cells revealed that alpha-santalol induces a strong apoptosis as early as 3 h post-treatment, which increases further in a concentration- and a time-dependent manner up to 12 h. 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. |
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 |
| 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. Dual staining with propidium iodide and Annexin V followed by flow cytometric analysis showed that TG facilitated cell death with clear necrotic characteristics. TG induced elevated ROS levels and suppressed caspase-3 in apoptotic cells pretreated for 24 h with cycloheximide. |
1(0,0,0,1) | Details |
| 16954565 | Tait JF, Smith C, Levashova Z, Patel B, Blankenberg FG, Vanderheyden JL: Improved detection of cell death in vivo with annexin V radiolabeled by site-specific methods. J Nucl Med. 2006 Sep;47(9):1546-53. |
8(0,0,0,8) | Details |
| 15809489 | Yagle KJ, Eary JF, Tait JF, Grierson JR, Link JM, Lewellen B, Gibson DF, Krohn KA: Evaluation of 18F-annexin V as a PET imaging agent in an animal model of apoptosis. J Nucl Med. 2005 Apr;46(4):658-66. METHODS: Annexin V was radiolabeled with 18F using N-succinimidyl-4-18F-fluorobenzoic acid chemistry, to a specific activity of 555-925 kBq/mug of protein. 18F-Annexin V (14.8-51.8 MBq) was administered intravenously to rats after pretreatment with cycloheximide (5 mg/kg) to induce liver apoptosis, and the injected rats were imaged by PET over 2 h. |
19(0,0,2,9) | Details |
| 15872355 | Tait JF, Smith C, Blankenberg FG: Structural requirements for in vivo detection of cell death with 99mTc-annexin V. J Nucl Med. 2005 May;46(5):807-15. The same pattern was observed in animals treated with cycloheximide to induce apoptosis. |
7(0,0,0,7) | Details |
| 16895761 | Baskic D, Popovic S, Ristic P, Arsenijevic NN: Analysis of cycloheximide-induced apoptosis in human leukocytes: fluorescence microscopy using annexin V/propidium iodide versus acridin orange/ethidium Cell Biol Int. 2006 Nov;30(11):924-32. Epub 2006 Jul 5. |
7(0,0,1,2) | 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. |
6(0,0,1,1) | 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 |
| 19222854 | Smith C, Gibson DF, Tait JF: Transmembrane voltage regulates binding of annexin V and lactadherin to cells with exposed BMC Biochem. 2009 Feb 17;10:5. |
3(0,0,0,3) | 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 |