Publication Date:
1990-03-02
Description:
Oncogenic activation of the proto-oncogene c-abl in human leukemias occurs as a result of the addition of exons from the gene bcr and truncation of the first abl exon. Analysis of tyrosine kinase activity and quantitative measurement of transformation potency in a single-step assay indicate that variation in bcr exon contribution results in a functional difference between p210bcr-abl and p185bcr-abl proteins. Thus, foreign upstream sequences are important in the deregulation of the kinase activity of the abl product, and the extent of deregulation correlates with the pathological effects of the bcr-abl proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lugo, T G -- Pendergast, A M -- Muller, A J -- Witte, O N -- 5T32GM07185/GM/NIGMS NIH HHS/ -- IT32GM08243/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 2;247(4946):1079-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2408149" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Blotting, Southern
;
Cell Line
;
*Cell Transformation, Neoplastic/genetics
;
Exons
;
*Gene Expression Regulation, Neoplastic
;
Leukemia, Experimental/genetics
;
Protein-Tyrosine Kinases/genetics/*metabolism
;
Proto-Oncogene Proteins/genetics/*metabolism
;
Proto-Oncogene Proteins c-abl
;
Proto-Oncogene Proteins c-bcr
;
Retroviridae/genetics
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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