Cellular interactions of CRKL, and SH2-SH3 adaptor protein
(1994) In Cancer Research 54(10). p.2563-2567- 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,... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1108695
- author
- ten Hoeve, J ; Kaartinen, V ; Fioretos, Thoas LU ; Haataja, L ; Voncken, J W ; Heisterkamp, N and Groffen, J
- publishing date
- 1994
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Cancer Research
- volume
- 54
- issue
- 10
- pages
- 2563 - 2567
- publisher
- American Association for Cancer Research Inc.
- external identifiers
-
- pmid:8168080
- scopus:0028301179
- ISSN
- 1538-7445
- language
- English
- LU publication?
- no
- id
- 75e25b84-ae57-4386-9092-2327d411dbd5 (old id 1108695)
- alternative location
- http://cancerres.aacrjournals.org/cgi/reprint/54/10/2563
- date added to LUP
- 2016-04-01 15:24:57
- date last changed
- 2021-01-04 15:50:46
@article{75e25b84-ae57-4386-9092-2327d411dbd5, 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.}}, author = {{ten Hoeve, J and Kaartinen, V and Fioretos, Thoas and Haataja, L and Voncken, J W and Heisterkamp, N and Groffen, J}}, issn = {{1538-7445}}, language = {{eng}}, number = {{10}}, pages = {{2563--2567}}, publisher = {{American Association for Cancer Research Inc.}}, series = {{Cancer Research}}, title = {{Cellular interactions of CRKL, and SH2-SH3 adaptor protein}}, url = {{http://cancerres.aacrjournals.org/cgi/reprint/54/10/2563}}, volume = {{54}}, year = {{1994}}, }