Cloning of the 3′ end of rat bax-α and corresponding developmental down-regulation in differentiating primary, cultured oligodendrocytes

• Published in: Neuroscience letters 1996-12, Vol.220 (3), p.183-186
• Main Authors: Madison, Dana L., Pfeiffer, Steven E.
• Format: Article
• Language: English
• Subjects: Amino Acid Sequence; Animals; Apoptosis; Base Sequence; bax-α; bcl; bcl-2-Associated X Protein; Biological and medical sciences; Blotting, Northern; cDNA sequence; Cell Differentiation - physiology; Cells, Cultured; Cloning, Molecular; Development; Down-Regulation - physiology; Fundamental and applied biological sciences. Psychology; Humans; Isolated neuron and nerve. Neuroglia; Mice; Molecular Sequence Data; Myelin; Neuroglia - metabolism; Oligodendrocyte; Oligodendroglia - metabolism; Oligodendroglia - physiology; Polymerase Chain Reaction; Proto-Oncogene Proteins - biosynthesis; Proto-Oncogene Proteins c-bcl-2; Rats; RNA, Messenger - biosynthesis; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(96)13263-8

Bax-α is thought to form heterodimers with Bcl-2 and prevent apoptotic cell death. A sequence was isolated from oligodendrocyte cDNA corresponding to the uncloned 3′ end of the rat bax-α coding region and part of the 3′ UTR via a degenerate polymerase chain reaction (PCR)-based cloning method. The rat bax-α clone is 96 and 91% homologous to mouse and human clones, respectively, and the 3′ UTR demonstrates high homology with the cloned human 3′ UTR. Northern analysis demonstrated that the 1.0 kb bax-ga mRNA species was predominant. bax-α mRNA is expressed in mitotic, oligodendrocyte progenitors, and is subsequently down-regulated 2-fold in differentiating oligodendrocytes.