Abstract：
:Chronic myelogenous leukemia is characterized by a specific chromosomal translocation, t(9;22), in which the ABL protooncogene and the BCR gene become juxtaposed. The chimeric BCR/ABL gene produces a P210 fusion protein with deregulated tyrosine kinase activity. We have recently isolated a complementary DNA, CRKL, which could code for an adaptor protein consisting of one SH2 and two SH3 domains and lacking any catalytic domain. In the current study, we show that CRKL is highly phosphorylated in the chronic myelogenous leukemia cell line K562 and that it is a substrate for the p210 BCR/ABL and p145 ABL kinases. BCR/ABL and ABL are coimmunoprecipitated with CRKL in vivo, demonstrating that relatively stable complexes are formed. In addition, the nucleotide exchange factor mSOS1 was found to be coimmunoprecipitated with CRKL. These findings establish a putative signal transduction pathway way through which BCR/ABL mediates its oncogenic activity.
journal_name
Cancer Resjournal_title
Cancer researchauthors
ten Hoeve J,Kaartinen V,Fioretos T,Haataja L,Voncken JW,Heisterkamp N,Groffen Jsubject
Has Abstractpub_date
1994-05-15 00:00:00pages
2563-7issue
10eissn
0008-5472issn
1538-7445journal_volume
54pub_type
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