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Jimmidi , R. and Reddy , B.R. and Satyanarayana , M. and Reddy , J. and Sawant , M.A. and Sitasawad , S.L. and Arya , P. and Mitra , P. (2014) Prevention of Mitochondrial Membrane Permeabilization and Prevention of Mitochondrial Membrane Permeabilization and Pancreatic β-Cell Death by an Enantioenriched, Macrocyclic Small Molecule. Eur. J. Org. Chem.. pp. 1151-1156.

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Mitochondria produce the majority of cellular energy through the process of oxidative phosphorylation and play a central role in regulating the functionality and survival of eukaryotic cells. Under physiological stress, mitochondrial membrane permeabilization results in the release of apoptogenic material such as cytochrome c in the cytoplasm, which thereby initiates caspase activation and the consequent cell death. In our present study, we screened a series of compounds for their ability to inhibit mitochondrial membrane permeabilization and to prevent cytochrome c release during the endoplasmic reticulum stress in cultured pancre-atic β-cells. Three benzofuran-based macrocyclic small molecules, that is, 2.4c, c104, and c108, were found to restore the depolarization of mitochondrial membrane potential and to prevent the release of cytochrome c from mitochondria. Interestingly, the acyclic precursor of 2.4c (i.e., 2.3c) did not show any effect, whereas the macrocyclic derivative obtained by utilizing ring-closing metathesis as the “stitching technology” led to this function. The macrocyclic architecture seems to play a crucial role in presenting various functional moieties in the right orientation to observe this effect.

Item Type: Article
Subjects: Cancer Biology
Depositing User: Mr. Rameshwar Nema
Date Deposited: 22 Apr 2015 08:45
Last Modified: 30 Jun 2015 11:19
URI: http://nccs.sciencecentral.in/id/eprint/98

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