PARP1
HGNC:270
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[ (||image_reduire{0,60}|inserer_attribut{alt,}) ] [ (||image_reduire{0,60}|inserer_attribut{alt,The AIF pathway of apoptosis}) ]
DNA damage elicits the activation of PARP1 (Poly[ADP-Ribose] Polymerase-1), a nuclear enzyme that facilitates DNA repair after injury, transferring ADP-ribose to nuclear proteins with consequent NADH depletion to very low levels.
Hence, there is decreased NADH oxidase activity by AIF since there is little or no NADH available to be oxidized.
Under those specific conditions, AIF might accept electrons from a source other than NADH, such as a potentially toxic free radical or H2O2, and thus act as a scavenger.
This redox cycling (alternate accepting and donating an electron), can serve as a protective mechanism.
Decrement in NAD+ is also perceived by the mitochondria, leading to translocation of AIF to the nucleus and initiation of nuclear condensation.
If these or similar conditions hold, then the oxidoreductase activity of AIF would be antiapoptotic while its DNA binding activity would be proapoptotic, resulting in dueling functions of different regions of AIF with potentially different outcomes dependent on cell type and insult.
See also
base excision repair (BER system of DNA repair)