Evans C A, Owen-Lynch P J, Whetton A D, Dive C
CRC Molecular and Cellular Pharmacology Group, Manchester University School of Biological Sciences, United Kingdom.
Cancer Res. 1993 Apr 15;53(8):1735-8.
A chromosomal translocation uniquely associated with chronic myeloid leukemia leads to the formation of a chimeric gene, bcr-abl, on the Philadelphia chromosome. The BRC-ABL protein displays an uncontrolled tyrosine kinase activity similar to that seen with the transforming oncogene of the Abelson murine leukemia (ABL) virus (v-abl). An interleukin 3 dependent cell line, IC.DP, has been transfected with a gene encoding a temperature sensitive v-ABL. In the absence of interleukin 3 at the restrictive temperature for ABL tyrosine kinase activity IC.DP cells died via apoptosis. At the permissive temperature ABL tyrosine kinase activity promoted IC.DP cell survival but not proliferation. ABL therefore can specifically suppress apoptosis.
一种与慢性粒细胞白血病独特相关的染色体易位导致了费城染色体上嵌合基因bcr-abl的形成。BRC-ABL蛋白表现出不受控制的酪氨酸激酶活性,类似于阿贝尔森鼠白血病(ABL)病毒(v-abl)的转化癌基因所具有的活性。一种依赖白细胞介素3的细胞系IC.DP已被转染了编码温度敏感型v-ABL的基因。在ABL酪氨酸激酶活性的限制温度下,缺乏白细胞介素3时,IC.DP细胞通过凋亡死亡。在允许温度下,ABL酪氨酸激酶活性促进了IC.DP细胞的存活,但不促进其增殖。因此,ABL可以特异性地抑制凋亡。