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10.1016/j.bbabio.2010.10.023 http://scihub22266oqcxt.onion/10.1016/j.bbabio.2010.10.023 C4681500!4681500!21074512     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochim+Biophys+Acta 2011 ; 1807 (6): 620-5 Nephropedia Template TP {{tp|p=21074512|t=2011. Genetic insights into OXPHOS defect and its role in cancer |pdf=|usr=}}{{21074512}} gab.com Text Genetic insights into OXPHOS defect and its role in cancer JO: Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=21074512 #FOAvip Warburg proposed that cancer originates from irreversible injury to mitochondrial oxidative phosphorylation (mtOXPHOS), which leads to an increase rate of aerobic glycolysis in most cancers. However, despite several decades of research related to Warburg effect, very little is known about the underlying genetic cause(s) of mtOXPHOS impairment in cancers. Proteins that participate in mtOXPHOS are encoded by both mitochondrial DNA (mtDNA) as well as nuclear DNA. This review describes mutations in mtDNA and reduced mtDNA copy number, which contribute to OXPHOS defects in cancer cells. Maternally inherited mtDNA renders susceptibility to cancer, and mutation in the nuclear encoded genes causes defects in mtOXPHOS system. Mitochondria damage checkpoint (mitocheckpoint) induces epigenomic changes in the nucleus, which can reverse injury to OXPHOS. However, irreversible injury to OXPHOS can lead to persistent mitochondrial dysfunction inducing genetic instability in the nuclear genome. Together, we propose that ?mitocheckpoint? led epigenomic and genomic changes must play a key role in reversible and irreversible injury to OXPHOS described by Warburg. These epigenetic and genetic changes underlie the Warburg phenotype, which contributes to the development of cancer. Twit Text FOAVip Genetic insights into OXPHOS defect and its role in cancer ????Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=21074512 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21074512 #FOAvip English Wikipedia <ref>{{Cite pmid|21074512}}</ref> Genetic insights into OXPHOS defect and its role in cancer #MMPMID21074512 Chandra D; Singh KK Biochim Biophys Acta 2011[Jun]; 1807 (6): 620-5 PMID21074512show ga Warburg proposed that cancer originates from irreversible injury to mitochondrial oxidative phosphorylation (mtOXPHOS), which leads to an increase rate of aerobic glycolysis in most cancers. However, despite several decades of research related to Warburg effect, very little is known about the underlying genetic cause(s) of mtOXPHOS impairment in cancers. Proteins that participate in mtOXPHOS are encoded by both mitochondrial DNA (mtDNA) as well as nuclear DNA. This review describes mutations in mtDNA and reduced mtDNA copy number, which contribute to OXPHOS defects in cancer cells. Maternally inherited mtDNA renders susceptibility to cancer, and mutation in the nuclear encoded genes causes defects in mtOXPHOS system. Mitochondria damage checkpoint (mitocheckpoint) induces epigenomic changes in the nucleus, which can reverse injury to OXPHOS. However, irreversible injury to OXPHOS can lead to persistent mitochondrial dysfunction inducing genetic instability in the nuclear genome. Together, we propose that ?mitocheckpoint? led epigenomic and genomic changes must play a key role in reversible and irreversible injury to OXPHOS described by Warburg. These epigenetic and genetic changes underlie the Warburg phenotype, which contributes to the development of cancer. äGenetic insights into OXPHOS defect and its role in cancer (epmc).pdf DeepDyve Pubget Overpricing