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

  title={PARP-1--a Perpetrator of Apoptotic Cell Death?},
  author={Alberto Chiarugi and Michael A. Moskowitz},
  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. 
Dueling Activities of AIF in Cell Death versus Survival DNA Binding and Redox Activity
Apoptosis-inducing factor (AIF) was originally discovered as a mitochondrial protein that, like cytochrome c, is released into the cytoplasm during cell death. New evidence suggests, however, that aExpand
Poly(ADP-ribose) polymerase-1 and apoptosis inducing factor in neurotoxicity
PARP-1 activation signals AIF release from the mitochondria, resulting in a novel, caspase-independent pathway of programmed cell death, suggesting that AIF maybe a target for development of future therapeutic treatment for many neurological disorders involving excitotoxicity. Expand
Apoptosis: Insights into Pathways and Role of p53, Bcl-2 and Sphingosine Kinases
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. Expand
Thioredoxin reduces post‐ischemic myocardial apoptosis by reducing oxidative/nitrative stress
  • L. Tao, E. Gao, +6 authors X. Ma
  • Chemistry, Medicine
  • British journal of pharmacology
  • 2006
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.
Several lines of evidence suggest that this pathway plays a role in I/R injury, although some studies indicate that mitochondrial dysfunction may also trigger AIF translocation and cell death, although the exact mechanisms linking PARP-1 and AIF in the induction of the ROS-induced cell death are still unclear. Expand
Molecular Tweezers Inhibit PARP‐1 by a New Mechanism
Inhibition of the key enzyme for DNA quality control, i.e. PARP-1, by synthetic molecular tweezers is demonstrated via a non-competitive mechanism with an IC50 value of 3 µM. Electrophoretic mobilityExpand
Cul 4 a as a New Interaction Protein of PARP 1 Inhibits Oxidative Stress-Induced H 9 c 2 Cell Apoptosis
Oxidative stress plays a major part in myocardial reperfusion injury. Cul4a is the core protein of CRLs E3 ubiquitin ligase complex; while it is known that Cul4a is responsible for various cancers,Expand
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. Expand
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. Expand
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. Expand


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. Expand
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. Expand
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. Expand
Apoptosis-regulating proteins as targets for drug discovery.
Knowledge of the molecular details of apoptosis regulation, and the three-dimensional structures of proteins constituting the apoptosis core machinery has revealed new strategies for identifying small-molecule drugs that could one day yield more effective treatments for a wide variety of illnesses. Expand
Apoptosis-inducing factor (AIF): a novel caspase-independent death effector released from mitochondria.
Data suggest that AIF plays a role in the regulation of caspase-independent cell death, which is essential for programmed cell death during cavitation of embryoid bodies. Expand
Poly(ADP-ribose) polymerase: killer or conspirator? The 'suicide hypothesis' revisited.
  • A. Chiarugi
  • Biology, Medicine
  • Trends in pharmacological sciences
  • 2002
The hypothesis that PARPs might regulate cell fate as essential modulators of death and survival transcriptional programs will be discussed with particular focus on the regulation of transcription factors such as nuclear factor kappaB and p53. Expand
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. Expand
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. Expand
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. Expand
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. Expand