Lin E Y, Orlofsky A, Wang H G, Reed J C, Prystowsky M B
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10467, USA.
Blood. 1996 Feb 1;87(3):983-92.
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.
A1是一种bcl-2家族成员，已被鉴定为造血特异性早期诱导基因。本研究表明，将A1稳定转染至依赖白细胞介素-3（IL-3）的髓系前体细胞系32D c13中，会导致IL-3撤除诱导的细胞死亡延迟，这与转染bcl-2时观察到的情况相似。然而，与bcl-2不同的是，A1的表达允许在IL-3撤除之前和之后分化的髓系细胞积累。另一方面，在IL-3剥夺后，bcl-2转染细胞中的总细胞积累比表达A1的细胞要多得多。与这两个基因共转染的细胞与单独转染bcl-2的细胞表现相似，只是IL-3撤除后的活力有所进一步增强。这些结果表明，这两种蛋白质具有不同的作用，这可能与其在髓系分化过程中表达的不同调控有关。
