Enhancement of peroxynitrite-induced apoptosis in PC12 cells by fibroblast growth factor-1 and nerve growth factor requires p21Ras activation and is suppressed by Bcl-2.
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Summary
The results indicate that the enhancement of peroxynitrite-induced apoptosis caused by NGF and FGF-1 is dependent on the stimulation of a proapoptotic pathway involving p21Ras that can be suppressed by Bcl-2.
- Type
- article
- Published
- 1998-08-01
- Cited by
- 38
- References
- 30
- OpenAlex
- https://openalex.org/W1978679885
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:2136200
Keywords
Peroxynitrite, Nerve growth factor, Apoptosis, Cell biology, Fibroblast growth factor
References
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- Peroxynitrite oxidation of sulfhydryls. The cytotoxic potential of superoxide and nitric oxide.
- Aconitase is readily inactivated by peroxynitrite, but not by its precursor, nitric oxide.
- The apoptosis endonuclease and its regulation.
- Effect of a dominant inhibitory Ha-ras mutation on neuronal differentiation of PC12 cells
- Acidic and basic fibroblast growth factors promote stable neurite outgrowth and neuronal differentiation in cultures of PC12 cells
- Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked
- Sensitivity of the essential zinc-thiolate moiety of yeast alcohol dehydrogenase to hypochlorite and peroxynitrite.
- FAS-induced apoptosis is mediated via a ceramide-initiated RAS signaling pathway.
- Phosphorylation of Bcl-2 Protein and Association with p21Ras in Ras-induced Apoptosis (*)
- Bcl-2 functions in an antioxidant pathway to prevent apoptosis.
- Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor.
- Peroxynitrite-mediated tyrosine nitration catalyzed by superoxide dismutase.
- Colocalization of NOS and SOD1 in neurofilament accumulation within motor neurons of amyotrophic lateral sclerosis: an immunohistochemical study.
- Induction of nitrotyrosine-like immunoreactivity in the lower motor neuron of amyotrophic lateral sclerosis.
- Transducing signals of life and death.
- Peroxynitrite causes apoptosis in rat thymocytes.
Cited by
- Cellular Signaling Pathways in Neuronal Apoptosis
- On the role of the inducible enzymes iNOS and COX-2 in colitis
- Oxidative‐stress‐dependent up‐regulation of Bcl‐2 expression in the central nervous system of aged Fisher‐344 rats
- Regulation of Growth and Differentiation in Early Mammalian Embryo by FGF and NGF Growth Factors in Organ Culture in Vitro
- Free radical‐dependent nuclear localization of Bcl‐2 in the central nervous system of aged rats is not associated with Bcl‐2‐mediated protection from apoptosis
- Nitric oxide and peroxynitrite. The ugly, the uglier and the not so good: a personal view of recent controversies.
- Peroxynitrite-induced cytotoxicity: mechanism and opportunities for intervention.
- Nitration of Hsp90 induces cell death
- Prevention of Peroxynitrite-induced Apoptosis of Motor Neurons and PC12 Cells by Tyrosine-containing Peptides*
- Mutations in signal transduction proteins increase stress resistance and longevity in yeast, nematodes, fruit flies, and mammalian neuronal cells.
- Peroxynitrite modulates the activation of p38 and extracellular regulated kinases in PC12 cells.
- Novel anti‐apoptotic effect of Bcl‐2: Prevention of polyamine depletion‐induced cell death
- GDNF improves cerebellar Purkinje neuron function in aged F344 rats
- Ethanol-induced alterations in the expression of neurotrophic factors in the developing rat central nervous system.
- Protective effects of IRFI-042 in monensin induced neurotoxicity in chicks.
- Expression and activity of 2-5A synthetase in the course of differentiation and apoptosis of PC12 cells.
- BCL-2 protects peroxynitrite-treated thymocytes from poly(ADP-ribose) synthase (PARS)-independent apoptotic but not from PARS-mediated necrotic cell death.
- Tyrosine nitration as mediator of cell death
- Inhibition of Caspase-Mediated Apoptosis by Peroxynitrite in Traumatic Brain Injury
- Nitric oxide synthase regulation and diversity: implications in Parkinson's disease.
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