carbocyanines and pifithrin

carbocyanines has been researched along with pifithrin* in 1 studies

Other Studies

1 other study(ies) available for carbocyanines and pifithrin

Article	Year
p53-mediated mitochondrial dysfunction by proteasome inhibition in dopaminergic SH-SY5Y cells. Neuroscience letters, 2004, Jan-16, Volume: 354, Issue:3 Decreased proteasome activity is an important pathology in Parkinson's disease (PD), which is related to cell death and Lewy body formation. In this study, we show that p53-activity may correlate with neuronal death via the mitochondrial pathway in PD model. The proteasome inhibitor, MG132, induced the accumulation of p53 in human dopaminergic neuroblastoma SH-SY5Y cells. The increased stabilization of p53 upregulated the level of Bax and mitochondrial depolarization. These events were inhibited by the p53 inhibitor, pifithrin-alpha (PFT). Cell viability analyzes demonstrated that PFT partially prevented MG132-induced cell death. These results suggest that p53 is a candidate as an intermediary between the proteasome system and mitochondria-related neuronal death in PD. Topics: bcl-2-Associated X Protein; Benzimidazoles; Benzothiazoles; Blotting, Western; Carbocyanines; Cell Death; Cell Line, Tumor; Cell Survival; Cysteine Endopeptidases; Cysteine Proteinase Inhibitors; Dopamine; Dose-Response Relationship, Drug; Drug Interactions; Fluorescent Antibody Technique; Humans; Leupeptins; Membrane Potentials; Mitochondria; Multienzyme Complexes; Neuroblastoma; Proteasome Endopeptidase Complex; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; Thiazoles; Time Factors; Toluene; Tumor Suppressor Protein p53	2004

Article

Year

p53-mediated mitochondrial dysfunction by proteasome inhibition in dopaminergic SH-SY5Y cells.

Neuroscience letters, 2004, Jan-16, Volume: 354, Issue:3

Decreased proteasome activity is an important pathology in Parkinson's disease (PD), which is related to cell death and Lewy body formation. In this study, we show that p53-activity may correlate with neuronal death via the mitochondrial pathway in PD model. The proteasome inhibitor, MG132, induced the accumulation of p53 in human dopaminergic neuroblastoma SH-SY5Y cells. The increased stabilization of p53 upregulated the level of Bax and mitochondrial depolarization. These events were inhibited by the p53 inhibitor, pifithrin-alpha (PFT). Cell viability analyzes demonstrated that PFT partially prevented MG132-induced cell death. These results suggest that p53 is a candidate as an intermediary between the proteasome system and mitochondria-related neuronal death in PD.

Topics: bcl-2-Associated X Protein; Benzimidazoles; Benzothiazoles; Blotting, Western; Carbocyanines; Cell Death; Cell Line, Tumor; Cell Survival; Cysteine Endopeptidases; Cysteine Proteinase Inhibitors; Dopamine; Dose-Response Relationship, Drug; Drug Interactions; Fluorescent Antibody Technique; Humans; Leupeptins; Membrane Potentials; Mitochondria; Multienzyme Complexes; Neuroblastoma; Proteasome Endopeptidase Complex; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; Thiazoles; Time Factors; Toluene; Tumor Suppressor Protein p53

2004