Title : Mitochondrial ND5 mutation mediated elevated ROS regulates apoptotic pathway epigenetically in a P53 dependent manner for generating pro-cancerous phenotypes.

Pub. Date : 2017 Jul

PMID : 28502718






3 Functional Relationships(s)
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1 Mitochondrial ND5 mutation mediated elevated ROS regulates apoptotic pathway epigenetically in a P53 dependent manner for generating pro-cancerous phenotypes. Reactive Oxygen Species tumor protein p53 Homo sapiens
2 Cells over-expressing mtND5 variant produced both peroxide as well as super-oxide ROS; the generation of which was dependent on the functional status of P53; modulating epigenetically the expression of key apoptosis pathway genes. Reactive Oxygen Species tumor protein p53 Homo sapiens
3 We propose that somatic mutation in mtND5 resulting in down-regulated complex I enzyme activity, elevated ROS and up-regulation of a set of nuclear anti-apoptotic genes epigenetically in the P53 dysfunctional cellular background, has provided a unique understanding of the molecular mechanism of mitochondrial mutation; and the concomitant existence of somatically acquired mitochondrial and nuclear p53 mutations, in cancer progression and promotion. Reactive Oxygen Species tumor protein p53 Homo sapiens