Wang J Y
Department of Biology, University of California, San Diego, La Jolla, 92093.
Oncogene Res. 1988;3(3):293-8.
Activation of the oncogenic potential of c-abl proto-oncogene has been correlated with the activation of its tyrosine kinase activity. The oncogenes derived from c-abl, e.g., gag/v-abl in Abelson murine leukemia virus or bcr/abl in chronic myelogenous leukemia, lack N-terminal coding sequences of the normal c-abl gene. In mouse and human cells, two sets of N-terminal amino acids encoded by 5'-variable exons are found in c-abl proteins. To assess the importance of N-terminal deletion in the activation of c-abl tyrosine kinase, a full length or an N-terminal deleted c-abl protein was expressed in bacteria and in monkey COS cells. Measurements of the autokinase activity of these two c-abl proteins showed that deletion of the N-terminal amino acids led to a three to five fold increase of the c-abl tyrosine kinase activity. Thus, the N-terminal deletion is important in the activation of c-abl proto-oncogene.
c-abl原癌基因致癌潜能的激活与其酪氨酸激酶活性的激活相关。源自c-abl的癌基因，例如艾贝尔森鼠白血病病毒中的gag/v-abl或慢性粒细胞白血病中的bcr/abl，缺乏正常c-abl基因的N端编码序列。在小鼠和人类细胞中，c-abl蛋白中发现了由5'-可变外显子编码的两组N端氨基酸。为了评估N端缺失在c-abl酪氨酸激酶激活中的重要性，在细菌和猴COS细胞中表达了全长或N端缺失的c-abl蛋白。对这两种c-abl蛋白的自身激酶活性的测量表明，N端氨基酸的缺失导致c-abl酪氨酸激酶活性增加了三到五倍。因此，N端缺失在c-abl原癌基因的激活中很重要。
