Abstract
The bcl-2 oncogene product delays apoptotic cell death and prolongs the cell survival. We cloned two bcl-2-related cDNAs from a rat thymus cDNA library by low stringency hybridization with a rat bcl-2 fragment as a probe. One of these, designated bcl-xalpha, was a counterpart of the human bcl-xL reported previously as a bcl-2-related gene (Boise, L. H., Gonzalez-Garcia, M., Postema, C. E. , Ding, L., Lindsten, T., Turka, L. A., Mao, M., Nunez, G., and Thompson, C. B. (1993) Cell 74, 597-608). The other, designated bcl-xbeta, was novel and found to be generated by an unspliced mRNA, whereas bcl-xalpha was generated from a spliced transcript. The splice junction exactly corresponded to that found in the bcl-2 gene. bcl-xbeta was specifically expressed in cerebellum, heart, and thymus. When bcl-xbeta directed by a strong promoter was introduced into an interleukin-3-dependent promyeloid cell line, FDC-P1, DNA fragmentation was observed even in the growing state in the presence of interleukin-3 although not in the control transfectants. This finding suggests that the rat bcl-xbeta gene product promotes apoptosis in the promyeloid cells.
Highlights
Bcl-2-related cDNAs from a rat thymus cDNA library by protein, which is considered to be responsible for Alzheimer’s low stringency hybridization with a rat bcl-2 fragment as a probe
Isolation of a Rat bcl-2 Fragment and Screening—A fragment of rat bcl-2 was amplified by polymerase chain reaction (PCR) (Saiki et al, 1990) using primers sequences that were common between mouse and human bcl-2s (5Ј-ATGGCGCACGCTGGGAGAA and 5Ј-CCTGGATCCAGGTGTGCAG)
Isolation of Rat bcl-x cDNAs—Overexpression of the bcl-2 gene delays apoptotic cell death in some but not in all cultured cells. These findings suggest the presence of multiple pathways of apoptosis
Summary
Bcl-2-related cDNAs from a rat thymus cDNA library by protein, which is considered to be responsible for Alzheimer’s low stringency hybridization with a rat bcl-2 fragment as a probe. When bcl-x directed by a strong promoter was introduced into an interleukin-3-dependent promyeloid cell line, FDC-P1, DNA fragmentation was observed even in the growing state in the presence of interleukin-3 not in the control transfectants This finding suggests that the rat bcl-x gene product promotes apoptosis in the promyeloid cells. In neuronal (Williams et al, 1990), treatment with some anticancer cells, apoptosis in ciliary neurons by withdrawal of ciliary neurotrophic factor was not delayed by introduction of the bcl-2 gene (Allsopp et al, 1993). These observations suggest the presence of multiple pathways for apoptosis.
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