ARRESTED DEVELOPMENT - UNDERSTANDING V-ABL

The protein tyrosine kinase activity of the v-abl oncogene has been de monstrated to subvert the normal second messenger systems used by lymp hoid cells for growth and differentiation. Transformation of bone marr ow with the Abelson murine leukemia virus results in the appearance of B cell lineage cells arrested at the pre-B cell stage, Recent reports have characterized these cells expressing high v-abl kinase activity as deficient in detectable NF-kappa B DNA binding activity and low lev el RAG gene expression. These observations suggest that v-abl may be i nhibiting the differentiation of B cells by blocking these two crucial elements in the maturation pathway.