Mediation of Poly(ADP-Ribose) Polymerase-1-Dependent Cell Death by Apoptosis-Inducing Factor
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Summary
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.
- Type
- article
- Published
- 2002-07-12
- Cited by
- 1,906
- References
- 26
- OpenAlex
- https://openalex.org/W1966928113
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:22991897
Keywords
Poly ADP ribose polymerase, Apoptosis-inducing factor, Programmed cell death, Apoptosis, Mitochondrion
References
- TNF-Induced Signaling in Apoptosis
- Myocardial Postischemic Injury Is Reduced by PolyADPribose Polymerase-1 Gene Disruption
- NMDA But Not Non-NMDA Excitotoxicity is Mediated by Poly(ADP-Ribose) Polymerase
- Mitochondrial control of cell death
- The Mitochondrial Permeability Transition, Release of Cytochrome c and Cell Death
- Ischemic Brain Injury is Mediated by the Activation of Poly(ADP-Ribose)Polymerase
- Poly(ADP-ribose) polymerase-1: what have we learned from the deficient mouse model?
- Poly(ADP-ribose) polymerase activation mediates 1-methyl-4-phenyl-1, 2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism.
- Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity.
- Excitatory amino acid neurotoxicity and neurodegenerative disease.
- Structure and function of poly(ADP-ribose) polymerase
- Poly(ADP-ribose) polymerase is a mediator of necrotic cell death by ATP depletion.
- A novel assay for apoptosis. Flow cytometric detection of phosphatidylserine expression on early apoptotic cells using fluorescein labelled Annexin V.
- Poly(ADP-ribose) polymerase inhibition in oxidant-stressed endothelial cells prevents oncosis and permits caspase activation and apoptosis.
- Implication of Poly(ADP‐Ribose) Polymerase (PARP) in Neurodegeneration and Brain Energy Metabolism: Decreases in Mouse Brain NAD+ and ATP Caused by MPTP Are Prevented by the PARP Inhibitor Benzamide
- Poly(ADP-ribose) polymerase gene disruption renders mice resistant to cerebral ischemia
- Role of poly(ADP-ribose) synthetase in inflammation and ischaemia-reperfusion.
- Roles of poly(ADP-ribosyl)ation and PARP in apoptosis, DNA repair, genomic stability and functions of p53 and E2F-1.
- Poly(ADP-ribose) synthetase activation mediates mitochondrial injury during oxidant-induced cell death.
- PARP is important for genomic stability but dispensable in apoptosis.
Cited by
- Poly(ADP-ribose) polymerase-1 (PARP1) and p53 labelling index correlates with tumour grade in meningiomas.
- Mammalian longevity under the protection of PARP-1's multi-facets.
- Schwann cell chemokine receptors mediate HIV‐1 gp120 toxicity to sensory neurons
- Niacin and Carcinogenesis
- Excitotoxic degeneration of hypothalamic orexin neurons in slice culture.
- Mitochondrial Impairment in the Developing Brain After Hypoxia–Ischemia
- mCICR is required for As2O3-induced permeability transition pore opening and cytochrome c release from mitochondria
- Apoptosis-inducing factor: vital and lethal.
- Players in the PARP-1 cell-death pathway: JNK1 joins the cast.
- Plasticity of the central nervous system (CNS) following perinatal asphyxia: Does nicotinamide provide neuroprotection?
- Does Transduced p27 Induce Apoptosis in Human Tumor Cell Lines?
- Utilizing multiplex ligation-dependent probe amplification to detect novel x -linked microduplications which cause intellectual disability
- Niacin Deficiency Alters p53 Expression and Impairs Etoposide-Induced Cell Cycle Arrest and Apoptosis in Rat Bone Marrow Cells
- Excessive Activation of Poly(ADP-Ribose) Polymerase Contributes to Inherited Photoreceptor Degeneration in the Retinal Degeneration 1 Mouse
- Inhibition of the activity of poly (ADP-ribose) polymerase reduces heart ischaemia/reperfusion injury via suppressing JNK-mediated AIF translocation
- Causal role of apoptosis-inducing factor for neuronal cell death following traumatic brain injury.
- Necroptosis: a specialized pathway of programmed necrosis.
- Loss of Anti-Bax Function in Gerstmann-Sträussler-Scheinker Syndrome-Associated Prion Protein Mutants
- Octanoate and Decanoate Induce Apoptosis in 3T3-L1 Adipocytes
- Poly(ADP-ribose) Polymerase (PARP)-1-independent Apoptosis-inducing Factor (AIF) Release and Cell Death Are Induced by Eleostearic Acid and Blocked by α-Tocopherol and MEK Inhibition*
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