| Name | c Jun N terminal kinase (protein family or complex) |
|---|---|
| Synonyms | c Jun N terminal kinase; JNK; c Jun NH (2) terminal kinase; Jun N terminal kinase |
| Name | paraquat |
|---|---|
| CAS | 1,1′-dimethyl-4,4′-bipyridinium |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16687388 | Niso-Santano M, Moran JM, Garcia-Rubio L, Gomez-Martin A, Gonzalez-Polo RA, Soler G, Fuentes JM: Low concentrations of paraquat induces early activation of extracellular signal-regulated kinase 1/2, protein kinase B, and c-Jun N-terminal kinase 1/2 pathways: role of c-Jun N-terminal kinase in paraquat-induced cell death. Toxicol Sci. 2006 Aug;92(2):507-15. Epub 2006 May 9. |
112(1,2,2,2) | Details |
| 15155744 | Peng J, Mao XO, Stevenson FF, Hsu M, Andersen JK: The herbicide paraquat induces dopaminergic nigral apoptosis through sustained activation of the JNK pathway. J Biol Chem. 2004 Jul 30;279(31):32626-32. Epub 2004 May 20. Our data show that paraquat induces the sequential phosphorylation of c-Jun N-terminal kinase (JNK) and c-Jun and the activation of caspase-3 and sequential neuronal death both in vitro and in vivo. |
81(1,1,1,1) | Details |
| 17018646 | Ramachandiran S, Hansen JM, Jones DP, Richardson JR, Miller GW: Divergent mechanisms of paraquat, MPP+, and rotenone toxicity: oxidation of thioredoxin and caspase-3 activation. Toxicol Sci. 2007 Jan;95(1):163-71. Epub 2006 Oct 3. In this study, we show that paraquat specifically oxidized the cytosolic form of thioredoxin and activated Jun N-terminal kinase (JNK), followed by caspase-3 activation. |
31(0,1,1,1) | Details |
| 12492400 | Cheng WH, Zheng X, Quimby FR, Roneker CA, Lei XG: Low levels of glutathione peroxidase 1 activity in -deficient mouse liver affect c-Jun N-terminal kinase activation and p53 phosphorylation on Ser-15 in pro-oxidant-induced aponecrosis. Biochem J. 2003 Mar 15;370(Pt 3):927-34. Both Se-deficient GPX1 knockout (GPX1 (-/-)) and wild-type (WT) mice ( n =64) were pretreated with an intraperitoneal injection of Se (as selenite, 50 microg/kg body weight) 6 h before an intraperitoneal injection of paraquat (12.5 mg/kg). |
2(0,0,0,2) | Details |
| 19720829 | Lee KS, Iijima-Ando K, Iijima K, Lee WJ, Lee JH, Yu K, Lee DS: JNK/FOXO-mediated neuronal expression of fly homologue of peroxiredoxin II reduces oxidative stress and extends life span. J Biol Chem. 2009 Oct 23;284(43):29454-61. Epub 2009 Aug 31. Activation of c-Jun N-terminal kinase (JNK) signaling in neurons increases stress resistance and extends life span, in part through FOXO-mediated transcription in Drosophila. We found that Jafrac1 was expressed in the adult brain and induced by paraquat, a reactive species-generating chemical. |
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. Oxidative stress, c-Jun N-terminal kinase activation, and alpha-synuclein aggregation are each induced by PQ, but details of the cell death mechanisms involved remain unclear. |
1(0,0,0,1) | Details |
| 18538428 | Jimenez-Del-Rio M, Daza-Restrepo A, Velez-Pardo C: The cannabinoid CP55,940 prolongs survival and improves locomotor activity in Drosophila melanogaster against paraquat: implications in Parkinson's disease. Neurosci Res. 2008 Aug;61(4):404-11. Epub 2008 May 2. Moreover, Drosophila fed with (1-200 microM) SP600125, a specific inhibitor of the stress responsive Jun-N-terminal kinase (JNK) signaling, and 20 mM PQ increased survival percentage and movement function (i.e., climbing capability) when compared to flies only treated with PQ. |
1(0,0,0,1) | Details |
| 20345759 | Sun HN, Kim SU, Huang SM, Kim JM, Park YH, Kim SH, Yang HY, Chung KJ, Lee TH, Choi HS, Min JS, Park MK, Kim SK, Lee SR, Chang KT, Lee SH, Yu DY, Lee DS: Microglial peroxiredoxin V acts as an inducible anti-inflammatory antioxidant through cooperation with redox signaling cascades. J Neurochem. 2010 Mar 20. Unlike in stimulation of oxidative insults with paraquat and peroxide, Prx V expression is highly sensitive to LPS-stimulation in microglia. Reduction of ROS level by treatment with either oxidase (Nox) inhibitor or antioxidant ablates LPS-mediated Prx V upregulation in BV-2 microglial cells and is closely associated with the activation of the c-Jun N-terminal kinase (JNK) signaling pathway. |
1(0,0,0,1) | 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. Similar results were obtained when paraquat was substituted for heat stress. |
1(0,0,0,1) | Details |