| Article ID | Journal | Published Year | Pages | File Type | 
|---|---|---|---|---|
| 5501604 | Free Radical Biology and Medicine | 2017 | 38 Pages | 
Abstract
												Pharmacologic ascorbate forms H2O2, damages DNA and activates PARP. Activated PARP depletes NAD+, and therefore inhibited GAPDH activity, and ATP is depleted in neuroblastoma cells, leading to cell death. In the absence of PARP activation, fatal DNA damage accumulates and leads to cell death.82
											Keywords
												poly-ADP-ribosePARP3-MAhistone 2AxGLUT1HIFECARCHK2dehydroascorbateIVCPhosphatidylinositol 3-KinasesBRAFGAPDHPARPiASCkirsten rat sarcoma viral oncogeneKRASOCRPI3KFBSH2AXz-VADOLAPSRBCATETo3-methyladenineataxia telangiectasia mutatedNAD+/NADHROSHydrogen peroxideAdenosine TriphosphateATPAscorbateDNA damageEtoposidestandard deviationolaparibcheckpoint kinase 2ParATMDHAfetal bovine serumsulforhodamine BHypoxia induced factorPARP inhibitorOxygen consumption rateextracellular acidification rateNeuroblastomaH2O2poly-ADP ribose polymerasepoly-ADP-ribose polymeraseTCA cycletricarboxylic acid cycleCatalaseChloroquineSerum starvationglucose transporter 1glyceraldehyde 3-phosphate dehydrogenaseGlycolysisReactive oxygen species
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											Authors
												Enlong Ma, Ping Chen, Heather M. Wilkins, Tao Wang, Russell H. Swerdlow, Qi Chen, 
											