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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142 Citations
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142 Citations

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The aim of this mini-review is to provide a general overview on the process of apoptosis including pathways, regulation, the role of apoptotic events in health and disease as well as the roles of p53, Bcl-2 and sphingosine kinase-1 in apoptosis.

Thioredoxin reduces post‐ischemic myocardial apoptosis by reducing oxidative/nitrative stress

Thioredoxin (Trx) is an oxidoreductase that prevents free radical‐induced cell death in cultured cells. Here we assessed the mechanism(s) underlying the cardioprotective effects of Trx in vivo.

Poly(ADP-ribose) polymerase-1 mediated caspase-independent cell death after ischemia/reperfusion.

Molecular Tweezers Inhibit PARP‐1 by a New Mechanism

Electrophoretic mobility shift assays and molecular docking experiments point to a simultaneous inclusion of lysine side chains in the tweezers cavity and one phosphate arm to the central Zn2+ ion of the zinc finger thereby displacing DNA.

Cul 4 a as a New Interaction Protein of PARP 1 Inhibits Oxidative Stress-Induced H 9 c 2 Cell Apoptosis

The results indicate that Cul4a is a new protective factor involved in oxidative stress-induced cardiomyocyte injury and functions by tying and decreasing overactivated PARP1.

Tankyrase-1 overexpression reduces genotoxin-induced cell death by inhibiting PARP1

A cytoprotective function of tankyrase-1 mediated through altered NAD+ homeostasis and inhibition of PARP1 function is indicated, which appears to protect cells by preventing genotoxins from activatingPARP1-mediated reactions such as PARp1 automodification and NAD+ consumption.

Retraction Note to: 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.

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.
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