PARP-1--a Perpetrator of Apoptotic Cell Death?

@article{Chiarugi2002PARP1aPO,
  title={PARP-1--a Perpetrator of Apoptotic Cell Death?},
  author={Alberto Chiarugi and Michael A. Moskowitz},
  journal={Science},
  year={2002},
  volume={297},
  pages={200 - 201}
}
The caspase-dependent pathway of programmed cell death has been well documented. In their Perspective, Chiarugi and Moskowitz report on new findings ( Yu et al .) that reveal a caspase-independent pathway of apoptosis driven by the nuclear enzyme PARP-1. 

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Retraction Note to: Advanced oxidation protein products induce chondrocyte death through a redox-dependent, poly(ADP-ribose) polymerase-1-mediated pathway

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RETRACTED ARTICLE: Advanced oxidation protein products induce chondrocyte death through a redox-dependent, poly (ADP-ribose) polymerase-1-mediated pathway

Results in vitro demonstrated that AOPPs induced cell death in human chondrocyte through a redox-dependent pathway, including RAGE-mediated, NADPH oxidase-dependent ROS generation, and poly (ADP-ribose) polymerase-1 (PARP-1) activation.
...

References

SHOWING 1-10 OF 16 REFERENCES

BCL-2 family members and the mitochondria in apoptosis.

As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die, and it is argued that the amphipathic a-helical BH3 domain serves as a critical death domain in the pro-apoptotic members.

Mediation of Poly(ADP-Ribose) Polymerase-1-Dependent Cell Death by Apoptosis-Inducing Factor

It is shown that PARP-1 activation is required for translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus and that AIF is necessary for PARp-1–dependent cell death.

Energy Requirement for Caspase Activation and Neuronal Cell Death

Some recent findings are discussed, which suggest that cells may use diverging execution pathways, with different implications in neuropathology and therapy.

Apoptosis in the nervous system

The principal molecular components of the apoptosis programme in neurons include Apaf-1 (apoptotic protease-activating factor 1) and proteins of the Bcl-2 and caspase families, which regulate neuronal apoptosis through the action of critical protein kinase cascades.

Poly(ADP-ribosylation) and apoptosis.

The aim of this review is to discuss the possible involvement of poly(ADP-ribosylation) during apoptosis by dealing with general considerations on apoptosis, and further examining the correlation between NAD consumption and cell death, the regulation of poly-ribose metabolism in apoptotic cells and the use of enzyme cleavage as a marker of apoptosis.

Poly(ADP-ribose) Polymerase-1 in the Nervous System

Novel forms of PARP derived from distinct genes and lacking classic DNA-binding domains may have nonnuclear functions, perhaps linked to cellular energy dynamics.

Infection and the origins of apoptosis

The proposal is that apoptosis (as defined by these molecular pathways) arose in one or more of the first multicellular animals, where it played a role in assuring the `social' interactions between cells, based on survival factor signaling.