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2014 ; 171
(8
): 2000-16
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Parthanatos: mitochondrial-linked mechanisms and therapeutic opportunities
#MMPMID24684389
Fatokun AA
; Dawson VL
; Dawson TM
Br J Pharmacol
2014[Apr]; 171
(8
): 2000-16
PMID24684389
show ga
Cells die by a variety of mechanisms. Terminally differentiated cells such as
neurones die in a variety of disorders, in part, via parthanatos, a process
dependent on the activity of poly (ADP-ribose)-polymerase (PARP). Parthanatos
does not require the mediation of caspases for its execution, but is clearly
mechanistically dependent on the nuclear translocation of the
mitochondrial-associated apoptosis-inducing factor (AIF). The nuclear
translocation of this otherwise beneficial mitochondrial protein, occasioned by
poly (ADP-ribose) (PAR) produced through PARP overactivation, causes large-scale
DNA fragmentation and chromatin condensation, leading to cell death. This review
describes the multistep course of parthanatos and its dependence on PAR
signalling and nuclear AIF translocation. The review also discusses potential
targets in the parthanatos cascade as promising avenues for the development of
novel, disease-modifying, therapeutic agents.
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