A1, a Bcl-2 family member, prolongs cell survival and permits myeloid differentiation

• Published in: Blood Vol. 87; no. 3; pp. 983 - 992
• Main Authors: Lin, E Y, Orlofsky, A, Wang, H G, Reed, J C, Prystowsky, M B
• Format: Journal Article
• Language: English
• Published: United States 01.02.1996
• Subjects: Animals; Apoptosis - genetics; Base Sequence; Cell Differentiation - drug effects; Cell Differentiation - genetics; Cell Division - drug effects; Cell Line; Cell Line, Transformed; Chlorocebus aethiops; DNA-Binding Proteins - genetics; DNA-Binding Proteins - physiology; Granulocyte Colony-Stimulating Factor - pharmacology; Hematopoietic Stem Cells - cytology; Hematopoietic Stem Cells - drug effects; Hematopoietic Stem Cells - metabolism; Homeodomain Proteins; Interleukin-3 - pharmacology; Mice; Minor Histocompatibility Antigens; Molecular Sequence Data; Proto-Oncogene Proteins - physiology; Proto-Oncogene Proteins c-bcl-2; Recombinant Fusion Proteins - metabolism; Replication Protein C; Repressor Proteins; Saccharomyces cerevisiae Proteins; Transfection
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.v87.3.983.bloodjournal873983

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 c13, 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.