Deletion of the ABL SH3 domain reactivates de-oligomerized BCR-ABL for growth factor independence

被引：16

作者：

Maru, Y ^{[1
]}

Witte, ON ^{[1
]}

Shibuya, M ^{[1
]}

机构：

[1] UNIV CALIF LOS ANGELES, HOWARD HUGHES MED INST, LOS ANGELES, CA 90024 USA

来源：

FEBS LETTERS | 1996年 / 379卷 / 03期

关键词：

BCR-ABL; oligomerization; SH3; domain; IL-3; dependence; tyrosine phosphorylation; GRB-2;

D O I：

10.1016/0014-5793(95)01518-3

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Biological activities of BCR-ABL, an activated tyrosine kinase oncogene responsible for pathogenesis of human leukemias, can be completely inactivated by a deletion of the BCR aminoterminal sequence with a tetramerizing property (BCR-ABL Delta 1-40). We attempted several ways to restore the ability to induce growth factor independence to the de-oligomerized BCR-ABL Delta 1-40 and found that an additional deletion of the ABL SH3 domain could, In BCR-ABL Delta 1-40 reactivated by the SH3 deletion, transphosphoryation of other cellular proteins like p62 or SHC in vivo and autophosphorylation with recruitment of GRB-2 were also recovered.

引用

页码：244 / 246

页数：3

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