| Name | bcl 2 |
|---|---|
| Synonyms | Apoptosis regulator Bcl 2; B cell CLL/lymphoma 2; B cell lymphoma protein 2 alpha; B cell lymphoma protein 2 alpha isoform; BCL2; Bcl 2; B cell CLL/lymphoma 2s; B cell lymphoma protein 2 alphas… |
| Name | paraquat |
|---|---|
| CAS | 1,1′-dimethyl-4,4′-bipyridinium |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12714668 | Rotstein NP, Politi LE, German OL, Girotti R: Protective effect of on oxidative stress-induced apoptosis of retina photoreceptors. Invest Ophthalmol Vis Sci. 2003 May;44(5):2252-9. DHA blocked the paraquat-induced increase in Bax expression and remarkably upregulated Bcl-2 expression. |
34(0,1,1,4) | Details |
| 12654481 | Cheng WH, Quimby FW, Lei XG: Impacts of glutathione peroxidase-1 knockout on the protection by injected against the pro-oxidant-induced liver aponecrosis and signaling in -deficient mice. Free Radic Biol Med. 2003 Apr 1;34(7):918-27. The paraquat-mediated gene or protein expression of proapoptotic Bax, Bcl-w, and Bcl-X (S), cell survival/death factors GADD45, MDM2, c-Myc, and caspase-3 was upregulated, but that of antiapoptotic Bcl-2 was downregulated in the GPX1-/- mice vs. the WT mice. |
31(0,1,1,1) | Details |
| 18715146 | Ethell DW, Fei Q: Parkinson-linked genes and toxins that affect neuronal cell death through the Bcl-2 family. Antioxid Redox Signal. 2009 Mar;11(3):529-40. Oxidative stress induced by the neurotoxins MPTP, paraquat, maneb, and rotenone causes lipid peroxidation and protein misfolding that affects cell death through members of the Bcl-2 family. |
7(0,0,1,2) | Details |
| 18266926 | Fei Q, Ethell DW: Maneb potentiates paraquat neurotoxicity by inducing key Bcl-2 family members. J Neurochem. 2008 Mar 11. |
6(0,0,1,1) | 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. |
2(0,0,0,2) | Details |
| 17509817 | Kang X, Chen J, Xu Z, Li H, Wang B: Protective effects of Ginkgo biloba extract on paraquat-induced apoptosis of PC12 cells. Toxicol In Vitro. 2007 Sep;21(6):1003-9. Epub 2007 Feb 21. Moreover, EGb761 pretreatment evidently increased the numbers of tyrosine hydroxylase (TH) positive and bcl-2 positive cells and degraded the number of caspase-3 positive cells in PQ-injured PC12 cells, in comparison to the treatment with PQ alone. |
2(0,0,0,2) | Details |
| 16565407 | German OL, Miranda GE, Abrahan CE, Rotstein NP: is a mediator of apoptosis in retina photoreceptors. Invest Ophthalmol Vis Sci. 2006 Apr;47(4):1658-68. synthesis in cultures treated with the oxidant paraquat was evaluated with [3H] Apoptosis, mitochondrial membrane potential, and Bcl-2 expression were determined. |
3(0,0,0,3) | Details |
| 16237197 | Bloom SE, Lemley AT, Muscarella DE: Potentiation of apoptosis by heat stress plus pesticide exposure in stress resistant human B-lymphoma cells and its attenuation through interaction with follicular dendritic cells: role for c-Jun N-terminal kinase signaling. Toxicol Sci. 2006 Jan;89(1):214-23. Epub 2005 Oct 19. This is due to increases in the levels of Bcl-2 protein as well as survival signals generated through B-cell binding to follicular dendritic cells (FDC). Similar results were obtained when paraquat was substituted for heat stress. |
2(0,0,0,2) | Details |
| 10082077 | Bar-Peled O, Knudson M, Korsmeyer SJ, Rothstein JD: Motor neuron degeneration is attenuated in bax-deficient neurons in vitro. J Neurosci Res. 1999 Mar 1;55(5):542-56. Bax is the first member of the bcl-2 family shown to promote apoptosis. |
1(0,0,0,1) | Details |
| 11369509 | Rossi L, Marchese E, Lombardo MF, Rotilio G, Ciriolo MR: Increased susceptibility of -deficient neuroblastoma cells to oxidative stress-mediated apoptosis. Free Radic Biol Med. 2001 May 15;30(10):1177-87. However, molecular markers of apoptosis Bcl-2, p53, and caspase-3 were slightly affected in these cells. When -deficient cells were challenged with oxidative stress generated by paraquat or puromycin, they underwent a higher degree of apoptosis with respect to -adequate control cells. |
1(0,0,0,1) | Details |
| 11413228 | Ciriolo MR, Aquilano K, De Martino A, Carri MT, Rotilio G: Differential role of and in S-nitrosoglutathione-mediated apoptosis: a rationale for mild forms of familial amyotrophic lateral sclerosis associated with less active Cu,Zn superoxide dismutase mutants. J Neurochem. 2001 Jun;77(6):1433-43. Cytochrome c release from mitochondria, caspase 3 activation, p53 up-regulation, p21 cleavage and Bcl-2 modulation, all involved in the apoptotic process, were significantly less altered with respect to untransfected cells. On the other hand, H46R cells were as sensitive as SH-SY5Y cells to puromycin-induced apoptosis; furthermore, they were more susceptible to apoptosis elicited by the -generating drug paraquat and to cell necrosis provoked by t-butyl hydroperoxide. |
1(0,0,0,1) | Details |
| 17935786 | Olesen BT, Clausen J, Vang O: Characterization of the transcriptional profile in primary astrocytes after oxidative stress induced by Paraquat. Neurotoxicology. 2008 Jan;29(1):13-21. Epub 2007 Sep 1. The PQ (48 h)-induced expressions of genes identified in cDNA array were confirmed by Northern blot analysis, which revealed a statistical significant up-regulation of genes involved in oxidative stress, detoxification, and DNA repair/synthesis and includes heme oxygenase-1 (11-fold), NAD (P) H dehydrogenase (8-fold), glutathione S-transferase P (7-fold), -regulated 78-kDa protein (7-fold), -regulated 75-kDa protein (6-fold), and growth-arrest and DNA-damage-inducible protein 45 (4.5-fold) and minor changes for heat shock 10-kDa protein, NADPH-cytochrome P450 reductase, heme oxygenase-2, proliferating cell nuclear antigen, and Bcl-2-associated death promoter. |
1(0,0,0,1) | Details |
| 10759888 | Nanbu-Wakao R, Asoh S, Nishimaki K, Tanaka R, Ohta S: Bacterial cell death induced by human pro-apoptotic Bax is blocked by an RNase E mutant that functions in an anti-oxidant pathway. Genes Cells. 2000 Mar;5(3):155-67. BACKGROUND: Bax is a member of the Bcl-2 family and induces apoptosis of mammalian cells. RESULTS: We isolated a Bax-resistant mutant from E. coli cells that survive in the presence of paraquat, a generator of by screening a library constructed from the random insertion of a transposon. |
1(0,0,0,1) | Details |