A sequence-specific splicing activator, tra2beta, is up-regulated in response to nerve injury.

Abstract

Tra2beta is the first mammalian protein which is proved to activate mRNA splicing in sequence-specific manner. Following hypoglossal nerve injury, the expression of Tra2beta mRNA was elevated in injured motoneurons transiently. The up-regulation of Tra2beta mRNA was observed from post-operative day 3 to 21. In addition to the nerve injury in PNS, a brain lesion in CNS also enhanced the expression of Tra2beta mRNA. The present study could be the first observation showing that an expression of the sequence-specific splicing activator is enhanced in neuronal cells in response to nerve injury, and indicates that Tra2beta may participate in the control of injury-specific splicing patterns in order to express molecules which are necessary for regeneration.

• Authors: S Kiryu-Seo, N Matsuo, A Wanaka, S Ogawa, M Tohyama, H Kiyama
• Journal: Brain research. Molecular brain research (Brain Res Mol Brain Res) Vol. 62 Issue 2 Pg. 220-3 (Nov 20 1998) ISSN: 0169-328X [Print] Netherlands
• PMID: 9813338 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright 1998 Elsevier Science B.V.

Chemical References

• Nerve Tissue Proteins
• RNA-Binding Proteins
• Tra2b protein, rat
• Serine-Arginine Splicing Factors

Topics

• Animals
• Axotomy
• Dominance, Cerebral
• Gene Expression Regulation
• Hypoglossal Nerve (metabolism)
• Hypoglossal Nerve Injuries
• Male
• Medulla Oblongata (metabolism)
• Motor Neurons (metabolism)
• Nerve Regeneration (genetics)
• Nerve Tissue Proteins (biosynthesis, genetics)
• RNA Splicing
• RNA-Binding Proteins (biosynthesis, genetics)
• Rats
• Rats, Wistar
• Serine-Arginine Splicing Factors
• Temporal Lobe (metabolism)