| Name | CHOP |
|---|---|
| Synonyms | 75 kDa DNA pairing protein; FUS1; CHOP; FUS; FUS 1; FUS CHOP; FUS/ATF1fusion gene; FUS/CHOP fusion gene… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19129918 | Drexler HC: Synergistic apoptosis induction in leukemic cells by the phosphatase inhibitor salubrinal and proteasome inhibitors. PLoS One. 2009;4(1):e4161. Epub 2009 Jan 8. Salubrinal further aggravated ER-stress and proteotoxicity inflicted by the proteasome inhibitors on the leukemic cells since characteristic ER stress responses, such as ATF4 and CHOP synthesis, XBP1 splicing, activation of MAP kinases and eventually apoptosis were efficiently abrogated by the translational inhibitor cycloheximide. |
31(0,1,1,1) | Details |
| 17067731 | Kumagai K, Ando Y, Kiyosawa N, Ito K, Kawai R, Yamoto T, Manabe S, Teranishi M: Toxicoproteomic investigation of the molecular mechanisms of cycloheximide-induced hepatocellular apoptosis in rat liver. Toxicology. 2006 Dec 7;228(2-3):299-309. Epub 2006 Sep 29. A previous study showed that the transcriptional level of CHOP was highly increased in rat liver in which hepatocellular apoptosis was induced by cycloheximide (CHX) treatment. |
10(0,0,1,5) | Details |
| 17804721 | Endo H, Murata K, Mukai M, Ishikawa O, Inoue M: Activation of insulin-like growth factor signaling induces apoptotic cell death under prolonged hypoxia by enhancing endoplasmic reticulum stress response. Cancer Res. 2007 Sep 1;67(17):8095-103. IGFs and insulin enhanced the endoplasmic reticulum (ER) stress response as monitored by induction of the CCAAT/enhancer binding protein homologous protein (CHOP) proteins and the X box protein-1 splicing under hypoxic conditions, and this response was suppressed by inhibiting PI3K and mTOR activity. IGF-induced cell death under hypoxic conditions was prevented by treatment with cycloheximide, suggesting that de novo protein synthesis is required. |
2(0,0,0,2) | 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. Induction of ER stress is further confirmed by the increased expression of the ER stress-regulated genes CHOP, ATF4, and GRP78. 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. |
1(0,0,0,1) | Details |
| 19561079 | Tardito S, Isella C, Medico E, Marchio L, Bevilacqua E, Hatzoglou M, Bussolati O, Franchi-Gazzola R: The thioxotriazole (II) complex A0 induces endoplasmic reticulum stress and paraptotic death in human cancer cells. J Biol Chem. 2009 Sep 4;284(36):24306-19. Epub 2009 Jun 26. Cycloheximide inhibited the accumulation of ubiquitinylated proteins and hampered A0-induced cell death process. The occurrence of the UPR during A0-induced death process was shown by the increased abundance of spliced XBP1 mRNA, transient eIF2alpha phosphorylation, and a series of downstream events, including attenuation of global protein synthesis and increased expression of ATF4, CHOP, BIP, and GADD34. |
1(0,0,0,1) | Details |
| 16219389 | Fukushima T, Koide M, Ago Y, Baba A, Matsuda T: T-817MA, a novel neurotrophic agent, improves sodium nitroprusside-induced mitochondrial dysfunction in cortical neurons. Neurochem Int. 2006 Jan;48(2):124-30. Epub 2005 Oct 10. The effects of T-817MA on SNP-induced decrease in cell viability and SNP-induced increase in mitochondrial ROS production were blocked by cycloheximide. SNP-induced neuronal toxicity was accompanied by a decrease in mitochondrial transmembrane potential without an increase in the expression of CHOP and GRP78 mRNAs, endoplasmic reticulum stress makers. |
1(0,0,0,1) | Details |
| 16357160 | Nawrocki ST, Carew JS, Dunner K Jr, Boise LH, Chiao PJ, Huang P, Abbruzzese JL, McConkey DJ: Bortezomib inhibits PKR-like endoplasmic reticulum (ER) kinase and induces apoptosis via ER stress in human pancreatic cancer cells. Cancer Res. 2005 Dec 15;65(24):11510-9. Bortezomib increased expression of ER stress markers, CHOP and BiP, but inhibited PKR-like ER kinase and subsequent phosphorylation of eukaryotic initiation factor 2alpha (eif2alpha), both of which are key events in translational suppression. The translation inhibitor cycloheximide abrogated bortezomib-induced protein aggregation, caspase-4 processing, and all other characteristics of apoptosis. |
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. Dramatic increases in the mRNA levels of ATF3 and CHOP genes, both of which were reported to play roles in the ER stress-mediated apoptosis pathway, were observed from 1h after the CHX treatment. |
1(0,0,0,1) | Details |
| 18322149 | Croons V, Martinet W, Herman AG, De Meyer GR: Differential effect of the protein synthesis inhibitors puromycin and cycloheximide on vascular smooth muscle cell viability. J Pharmacol Exp Ther. 2008 Jun;325(3):824-32. Epub 2008 Mar 5. Puromycin-treated SMCs showed signs of endoplasmic reticulum (ER) stress, as demonstrated by CCAAT/enhancer-binding protein homologous protein (CHOP) protein expression, splicing of X-box-binding protein 1 mRNA, and phosphorylation of eukaryotic translation initiation factor 2alpha. |
1(0,0,0,1) | Details |