A1, a bcl-2 family member, has been identified as a hematopoietic- specific, early inducible gene. In this study it is shown that stable transfection of A1 into an interleukin-3 (IL-3)dependent myeloid precursor cell line, 32D cl3, leads to a retardation of IL-3 withdrawal-induced cell death similar to that observed with transfection of bcl-2. However, unlike bcl-2, A1 expression permits the accumulation of differentiated myeloid cells both before and after IL-3 withdrawal. Total cell accumulation, on the other hand, is considerably greater after IL-3 deprivation in the bcl-2 transfectant than in A1-expressing cells. Cells cotransfected with the two genes behave similarly to cells singly transfected with bcl-2, except that viability following IL-3 withdrawal is somewhat further enhanced. These results suggest that these two proteins have distinct roles that may be related to the divergent regulation of their expression during myeloid differentiation.
|Original language||English (US)|
|Number of pages||10|
|State||Published - Feb 1 1996|
All Science Journal Classification (ASJC) codes
- Cell Biology