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bcl-x is expressed in embryonic and postnatal neural tissues and functions to prevent neuronal cell death

Gonzalez-Garcia, M.
Ding, L.
O'Shea, S.
Boise, L. H.
Thompson, C. B.
Nunez, G.
Published in Proceedings of the National Academy of Sciences. 1995, vol. 92, no. 10, p. 4304-4308
Abstract Previous studies have implicated the bcl-2 protooncogene as a potential regulator of neuronal survival. However, mice lacking functional bcl-2 exhibited normal development and maintenance of the central nervous system (CNS). Since bcl-2 appears dispensable for neuronal survival, we have examined the expression and function of bcl-x, another member of the bcl-2 family of death regulatory genes. Bcl-2 is expressed in neuronal tissues during embryonic development but is down-regulated in the adult CNS. In contrast, Bcl-xL expression is retained in neurons of the adult CNS. Two different forms of bcl-x mRNA and their corresponding products, Bcl-xL and Bcl-x beta, were expressed in embryonic and adult neurons of the CNS. Microinjection of bcl-xL and bcl-x beta cDNAs into primary sympathetic neurons inhibited their death induced by nerve growth factor withdrawal. Thus, Bcl-x proteins appear to play an important role in the regulation of neuronal survival in the adult CNS.
Keywords Aging/ metabolismAnimalsAnimals, NewbornBrain/embryology/growth & development/ metabolismCell Death/ physiologyCells, CulturedDNA, ComplementaryEmbryonic and Fetal DevelopmentIn Situ HybridizationLiver/metabolismMicroinjectionsNeurons/ cytology/ metabolismOrgan SpecificityProto-Oncogene Proteins/ biosynthesisProto-Oncogene Proteins c-bcl-2RatsSpinal Cord/growth & development/ metabolismSuperior Cervical Ganglion/cytology/physiologybcl-X Protein
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PMID: 7753802
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