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

被引:102
作者
Lin, EY
Orlofsky, A
Wang, HG
Reed, JC
Prystowsky, MB
机构
[1] MONTEFIORE MED CTR,ALBERT EINSTEIN COLL MED,DEPT PATHOL,BRONX,NY 10467
[2] LA JOLLA CANC RES FDN,ONCOGENE & TUMOR SUPRESSOR GENES PROGRAM,CANC RES INST,LA JOLLA,CA 92037
[3] UNIV PENN,SCH ARTS & SCI,BIOL GRAD GRP,PHILADELPHIA,PA
关键词
D O I
10.1182/blood.V87.3.983.bloodjournal873983
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 cI3, 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 Al-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. (C) 1996 by The American Society of Hematology.
引用
收藏
页码:983 / 992
页数:10
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