Downregulation of bcr-abl expression and kinase activity but reciprically increased phosphorylation of specific proteins in STI-571 resistant K562 cells: Evidence for the involvement of other tyrosine phosphoproteins in signaling and survival.

被引：0

|

作者：

Talpaz, M

Wu, JY

Kantarjian, H

Zhang, L

Gallick, GE

Kraker, AJ

Donato, NJ

机构：

[1] Univ Texas, MD Anderson Canc Ctr, Dept Bioimmunotherapy, Houston, TX 77030 USA

[2] Univ Texas, MD Anderson Canc Ctr, Dept Hematol, Houston, TX 77030 USA

[3] Univ Texas, MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA

[4] Pfizer Global Res & Dev, Ann Arbor, MI USA

来源：

BLOOD | 2000年 / 96卷 / 11期

关键词：

D O I：

暂无

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

1488

引用

收藏

页码：345A / 345A

页数：1

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[2] Novel tyrosine kinase inhibitors suppress BCR-ABL signaling and induce apoptosis in STI-571 sensitive and resistant CML cells.
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[3] A novel pyridopyrimidine inhibitor of Abl kinase is a picomolar inhibitor of Bcr-Abl-driven K562 cells and is effective against STI571-resistant Bcr-Abl mutants
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[4] Bcr-Abl tyrosine kinase activity is responsible for the apoptosis resistant phenotype of K562 cells by blocking an event independent of the caspase activation pathway.
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