| Name | Calpains (protein family or complex) |
|---|---|
| Synonyms | calpain; calpains |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16412576 | Chen MJ, Yap YW, Choy MS, Koh CH, Seet SJ, Duan W, Whiteman M, Cheung NS: Early induction of calpains in rotenone-mediated neuronal apoptosis. Neurosci Lett. 2006 Apr 10-17;397(1-2):69-73. Epub 2006 Jan 10. |
125(0,4,4,5) | Details |
| 17367952 | Samantaray S, Knaryan VH, Guyton MK, Matzelle DD, Ray SK, Banik NL: The parkinsonian neurotoxin rotenone activates calpain and caspase-3 leading to motoneuron degeneration in spinal cord of Lewis rats. Neuroscience. 2007 May 11;146(2):741-55. Epub 2007 Mar 23. |
87(1,1,2,2) | Details |
| 18673214 | Samantaray S, Ray SK, Banik NL: Calpain as a potential therapeutic target in Parkinson's disease. CNS Neurol Disord Drug Targets. 2008 Jun;7(3):305-12. In this review, we summarize the evidence in support of involvement of calpain, a Ca (2+)-activated non-lysosomal protease, in spinal cord degeneration in two models of experimental parkinsonism induced by the neurotoxin 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine and also the environmental toxin rotenone. |
35(0,1,1,5) | Details |
| 18991878 | Samantaray S, Butler JT, Ray SK, Banik NL: Extranigral neurodegeneration in Parkinson's disease. Ann N Y Acad Sci. 2008 Oct;1139:331-6. We examined the mechanisms of calpain-mediated neuronal death in differentiated spinal cord motoneuron cultures following exposure to the active parkinsonian toxins 1-methyl-4-phenyl-pyridinium ion (MPP (+)) and rotenone and also tested the neuroprotective efficacy of calpeptin, a calpain inhibitor, in these cell culture models of experimental parkinsonism. |
33(0,1,1,3) | Details |
| 19224578 | Gill MB, Perez-Polo JR: Bax shuttling after rotenone treatment of neuronal primary cultures: effects on cell death phenotypes. J Neurosci Res. 2009 Jul;87(9):2047-65. The 100 microM rotenone treatment also resulted in an early increase in nuclear Bax levels followed by a subsequent increase in ER Bax levels and calpain-mediated cleavage of alpha-fodrin. |
31(0,1,1,1) | Details |
| 17105932 | Samantaray S, Ray SK, Ali SF, Banik NL: Calpain activation in apoptosis of motoneurons in cell culture models of experimental parkinsonism. Ann N Y Acad Sci. 2006 Aug;1074:349-56. In cell culture models of experimental parkinsonism, we examined the degeneration of ventral SC motoneuron cell line (VSC4.1) following exposure to two different toxins, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone. |
4(0,0,0,4) | Details |
| 12153473 | Poppe M, Reimertz C, Munstermann G, Kogel D, Prehn JH: -induced apoptosis of D283 medulloblastoma cells requires mitochondrial respiratory chain activity but occurs independently of caspases and is not sensitive to Bcl-xL overexpression. J Neurochem. 2002 Aug;82(3):482-94. Treatment with the complex I inhibitor rotenone, C2- or C8- induced cell death in D283 control cells, while rho- cells were significantly protected. These morphological alterations were associated with the activation of calpains. |
3(0,0,0,3) | Details |
| 9804614 | Leist M, Volbracht C, Fava E, Nicotera P: 1-Methyl-4-phenylpyridinium induces autocrine excitotoxicity, protease activation, and neuronal apoptosis. Mol Pharmacol. 1998 Nov;54(5):789-801. The neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and other mitochondrial inhibitors (e.g., rotenone or 3-nitropropionic acid) elicited apoptosis in cerebellar granule cell cultures via stimulation of autocrine excitotoxicity. Two classes of proteases were involved in the execution of cell death: caspases and calpains. |
1(0,0,0,1) | Details |
| 8229832 | Deutsch N, Weiss JN: ATP-sensitive K+ channel modification by metabolic inhibition in isolated guinea-pig ventricular myocytes. J Physiol. 1993 Jun;465:163-79. Isolated guinea-pig ventricular myocytes were metabolically inhibited in -free 1.8 mM Ca2+ Tyrode solution containing 9 microM rotenone and 0.9 microM carbonyl -p-trifluoromethoxyphenylhydrazone (FCCP) while recording unitary currents through K+ATP channels in cell-attached patches. |
0(0,0,0,0) | Details |