Abstract
Summary and Directions
A key area of research on the structure and function of v-abl will be the search for the substrates critical to cell transformation. As we have seen the mechanism of activation of v-abl depends upon truncation of the normal c-abl protein to generate a protein with detectable tyrosine kinase activity. Why this means of activation should result in a transforming protein with tropism for the lymphoid lineage in mice is unclear, particularly when we consider that a similar mechanism of activation of abl genes is involved in the stem cell disease CML in humans. It is also not clear why v-abl is more efficient than other tyrosine kinase oncogenes in relieving cells of their requirements for the growth factor IL-3. The mechanism and significance of that activity will be a focus of future efforts. Finally understanding of the role of v-abl in tumori-genesis will require identification and analysis of other cellular genes that may play essential roles in progression in A-MuLV disease.
The authors' support is provided by National Cancer Institute Grant CA-41302 and Training Grant CA-09135.
Get full access to this article
View all access options for this article.