The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Bcl-2 and Ca(2+)-mediated mitochondrial dysfunction in neural cell death.
A N Murphy; G Fiskum (Profiled Author: Gary M Fiskum)
MitoKor, San Diego, CA 92121, USA.
Biochemical Society symposium 1999;66():33-41.
Although altered Ca2+ homoeostasis is believed to be a primary cause of death for many cell types in response to toxic insults, the specific Ca(2+)-stimulated event responsible for directing cells down the death pathway has remained elusive. Recent publications support the hypothesis that mitochondrial Ca2+ sequestration is the critical event in induction of excitotoxic neuronal death. If similar pathways are involved in the induction of Ca(2+)-induced necrotic and apoptotic death, then agents that mimic the action of the anti-apoptotic protein Bcl-2 should be particularly useful. Our previous results provide evidence that Bcl-2 increases the maximal capacity of mitochondria to accumulate Ca2+ while providing resistance to Ca(2+)-induced respiratory damage. In addition, we have found that Bcl-2 can block Ca(2+)-ionophore-induced delayed cell death. These data predict that in response to a challenging mitochondrial Ca2+ load, Bcl-2-containing mitochondria would be capable of continuing bioenergetic function, potentially avoiding a catastrophic death signalling event.
1 Originating Grant
1 May 1995 - 31 December 2008
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
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