en
Scientific article
English

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

Publication date1995
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/ metabolism
  • Animals
  • Animals, Newborn
  • Brain/embryology/growth & development/ metabolism
  • Cell Death/ physiology
  • Cells, Cultured
  • DNA, Complementary
  • Embryonic and Fetal Development
  • In Situ Hybridization
  • Liver/metabolism
  • Microinjections
  • Neurons/ cytology/ metabolism
  • Organ Specificity
  • Proto-Oncogene Proteins/ biosynthesis
  • Proto-Oncogene Proteins c-bcl-2
  • Rats
  • Spinal Cord/growth & development/ metabolism
  • Superior Cervical Ganglion/cytology/physiology
  • bcl-X Protein
Affiliation Not a UNIGE publication
Citation (ISO format)
GONZALEZ-GARCIA, M. et al. bcl-x is expressed in embryonic and postnatal neural tissues and functions to prevent neuronal cell death. In: Proceedings of the National Academy of Sciences of the United States of America, 1995, vol. 92, n° 10, p. 4304–4308. doi: 10.1073/pnas.92.10.4304
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Identifiers
ISSN of the journal0027-8424
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