| Name | caspases (protein family or complex) |
|---|---|
| Synonyms | caspase; caspases |
| Name | paraquat |
|---|---|
| CAS | 1,1′-dimethyl-4,4′-bipyridinium |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17438367 | Gonzalez-Polo RA, Niso-Santano M, Ortiz-Ortiz MA, Gomez-Martin A, Moran JM, Garcia-Rubio L, Francisco-Morcillo J, Zaragoza C, Soler G, Fuentes JM: Relationship between autophagy and apoptotic cell death in human neuroblastoma cells treated with paraquat: could autophagy be a "brake" in paraquat-induced apoptotic death?. Autophagy. 2007 Jul-Aug;3(4):366-7. Epub 2007 Jul 26. Whereas caspase inhibition retarded cell death, autophagy inhibition accelerated the apoptotic cell death induced by paraquat. |
81(1,1,1,1) | Details |
| 18773310 | Chinta SJ, Rane A, Poksay KS, Bredesen DE, Andersen JK, Rao RV: Coupling endoplasmic reticulum stress to the cell death program in dopaminergic cells: effect of paraquat. Neuromolecular Med. 2008;10(4):333-42. Epub 2008 Sep 5. We demonstrate that paraquat triggers ER stress, cell dysfunction, and dopaminergic cell death. p23, a small co-chaperone protein, is cleaved during ER stress-induced cell death triggered by paraquat and blockage of the caspase cleavage site of p23 was associated with decreased cell death. |
32(0,1,1,2) | Details |
| 18253895 | Yang W, Tiffany-Castiglioni E: Paraquat-induced apoptosis in human neuroblastoma SH-SY5Y cells: involvement of p53 and mitochondria. J Toxicol Environ Health A. 2008;71(4):289-99. In addition, paraquat increased the activities of caspases 9 and 3. |
6(0,0,1,1) | Details |
| 17341480 | Gonzalez-Polo RA, Niso-Santano M, Ortiz-Ortiz MA, Gomez-Martin A, Moran JM, Garcia-Rubio L, Francisco-Morcillo J, Zaragoza C, Soler G, Fuentes JM: Inhibition of paraquat-induced autophagy accelerates the apoptotic cell death in neuroblastoma SH-SY5Y cells. Toxicol Sci. 2007 Jun;97(2):448-58. Epub 2007 Mar 6. Finally, the cells succumbed to cell death with hallmarks of apoptosis such as exposure, caspase activation, and chromatin condensation. |
2(0,0,0,2) | Details |
| 10224137 | Lin KI, Pasinelli P, Brown RH, Hardwick JM, Ratan RR: Decreased intracellular levels activate Sindbis virus-induced apoptosis. J Biol Chem. 1999 May 7;274(19):13650-5. Infection of many cultured cell types with Sindbis virus (SV), an alphavirus, triggers apoptosis through a commonly utilized caspase activation pathway. Moreover, increasing intracellular O-2 by treatment of 3T3 cells with paraquat protects them from SV-induced death. |
2(0,0,0,2) | Details |
| 18190792 | Takamura A, Higaki K, Kajimaki K, Otsuka S, Ninomiya H, Matsuda J, Ohno K, Suzuki Y, Nanba E: Enhanced autophagy and mitochondrial aberrations in murine G (M1)-gangliosidosis. Biochem Biophys Res Commun. 2008 Mar 14;367(3):616-22. Epub 2008 Jan 9. These cells were more sensitive to oxidative stress than wild type cells and this sensitivity was suppressed by ATP, an autophagy inhibitor 3-methyladenine and a pan-caspase inhibitor z-VAD-fmk. |
1(0,0,0,1) | Details |
| 16580745 | Ross C, Santiago-Vazquez L, Paul V: Toxin release in response to oxidative stress and programmed cell death in the cyanobacterium Microcystis aeruginosa. Aquat Toxicol. 2006 Jun 10;78(1):66-73. Epub 2006 Apr 3. Despite the fact that secreted toxin levels were relatively low in dense natural assemblages (3.5 microg l (-1)), detectable toxin levels increased by 90% when M. aeruginosa was stressed by an increase in salinity, physical injury, application of the chemical herbicide paraquat, or UV irradiation. The application of micromolar concentrations of H (2) O (2) induced programmed cell death (PCD) as measured by a caspase protease assay. |
1(0,0,0,1) | Details |
| 11181820 | Chun HS, Gibson GE, DeGiorgio LA, Zhang H, Kidd VJ, Son JH: Dopaminergic cell death induced by MPP (+), oxidant and specific neurotoxicants shares the common molecular mechanism. J Neurochem. 2001 Feb;76(4):1010-21. Epidemiological risk factor analyses of typical PD cases have identified several neurotoxicants, including MPP (+) (the active metabolite of MPTP), paraquat, dieldrin, and Pharmacological intervention using the combination of the antioxidant Trolox and a pan-caspase inhibitor Boc-(Asp)-fmk (BAF) exerted significant neuroprotection against ROS-induced dopaminergic cell death. |
1(0,0,0,1) | Details |
| 19145491 | Chinta SJ, Poksay KS, Kaundinya G, Hart M, Bredesen DE, Andersen JK, Rao RV: Endoplasmic reticulum stress-induced cell death in dopaminergic cells: effect of J Mol Neurosci. 2009 Sep;39(1-2):157-68. Epub 2009 Jan 15. Earlier, we showed that paraquat, a bipyridyl herbicide, triggers endoplasmic reticulum stress, cell dysfunction, and dopaminergic cell death. Our studies demonstrate that triggers ER stress and cell dysfunction, caspase activation, p23 cleavage and inhibition of proteasomal activity in dopaminergic N27 cells. |
1(0,0,0,1) | Details |
| 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. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. |
1(0,0,0,1) | Details |
| 18365879 | Rio MJ, Velez-Pardo C: Paraquat induces apoptosis in human lymphocytes: protective and rescue effects of cannabinoids and insulin-like growth factor-1. Growth Factors. 2008 Feb;26(1):49-60. Further evaluation included (i) radicals, reflected by nitroblue tetrazolium reduction to formazan, (ii) the production of peroxide, reflected by rhodamine-positive fluorescent cells, (iii) the generation of reflected by dimethylsulfoxide and ( radical) OH scavengers, (iv) activation and/or translocation of NF-kappaB, p53 and c-Jun transcription factors showed by immunocytochemical staining, and by ammonium pyrrolidinedithiocarbamate, pifithrin-alpha and SP600125 inhibition and (V) caspase-3 activation, reflected by caspase Ac-DEVD-cho inhibition. |
1(0,0,0,1) | Details |
| 16497721 | Ravikumar B, Berger Z, Vacher C, O'Kane CJ, Rubinsztein DC: Rapamycin pre-treatment protects against apoptosis. Hum Mol Genet. 2006 Apr 1;15(7):1209-16. Epub 2006 Feb 23. Here, we show that rapamycin may have additional cytoprotective effects--it protects cells against a range of subsequent pro-apoptotic insults and reduces paraquat toxicity in Drosophila. This protection can be accounted for by enhanced clearance of mitochondria by autophagy, thereby reducing cytosolic cytochrome c release and downstream caspase activation after pro-apoptotic insults. |
1(0,0,0,1) | Details |
| 17561093 | Dinis-Oliveira RJ, Sousa C, Remiao F, Duarte JA, Ferreira R, Sanchez Navarro A, Bastos ML, Carvalho F: prevents paraquat-induced apoptosis in the rat lung. . Free Radic Biol Med. 2007 Jul 1;43(1):48-61. Epub 2007 Mar 24. The two main caspase cascades (the extrinsic receptor-mediated and the intrinsic mitochondria-mediated) and the expressions of p53 and activator protein-1 (AP-1) were also evaluated, to obtain an insight into apoptotic cellular signaling. |
1(0,0,0,1) | Details |