BAX Is Required for Neuronal Death after Trophic Factor Deprivation and during Development
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Abstract
References (65)
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A conserved domain in Bak, distinct from BH1 and BH2, mediates cell death and protein binding functions.
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bcl-2 protein expression is widespread in the developing nervous system and retained in the adult PNS
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bcl-2 deficiency in mice leads to pleiotropic abnormalities: accelerated lymphoid cell death in thymus and spleen, polycystic kidney, hair hypopigmentation, and distorted small intestine.
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NT-3 stimulates sympathetic neuroblast proliferation by promoting precursor survival
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Internucleosomal DNA cleavage and neuronal cell survival/death
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The protein bcl-2 alpha does not require membrane attachment, but two conserved domains to suppress apoptosis.
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Bax promotes neuronal survival and antagonises the survival effects of neurotrophic factors
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Function and expression of the Bcl-x gene in the developing and adult nervous system
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Naturally occurring and axotomy-induced motoneuron death and its prevention by neurotrophic agents: a comparison between chick and mouse
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Axotomized neonatal motoneurons overexpressing the bcl2 proto-oncogene retain functional electrophysiological properties.
1996 • 40 citations
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