Abstract
A fusion complementary DNA in the T cell line HSB-2 elucidates a provocative mechanism for the disruption of the putative hematopoietic transcription factor SCL . The fusion cDNA results from an interstitial deletion between a previously unknown locus, SIL ( SCL interrupting locus), and the 5′ untranslated region of SCL . Similar to 1;14 translocations, this deletion disrupts the SCL 5′ regulatory region. This event is probably mediated by V-(D)-J recombinase activity, although neither locus is an immunoglobulin or a T cell receptor. Two other T cell lines, CEM and RPMI 8402, have essentially identical deletions. Thus, in lymphocytes, growth-affecting genes other than immune receptors risk rearrangements.
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Dates
Type | When |
---|---|
Created | 18 years, 10 months ago (Oct. 5, 2006, 6:10 p.m.) |
Deposited | 1 year, 7 months ago (Jan. 12, 2024, 4:41 a.m.) |
Indexed | 2 months ago (June 26, 2025, 2:25 p.m.) |
Issued | 34 years, 8 months ago (Dec. 7, 1990) |
Published | 34 years, 8 months ago (Dec. 7, 1990) |
Published Print | 34 years, 8 months ago (Dec. 7, 1990) |
@article{Aplan_1990, title={Disruption of the Human SCL Locus by “Illegitimate” V-(D)-J Recombinase Activity}, volume={250}, ISSN={1095-9203}, url={http://dx.doi.org/10.1126/science.2255914}, DOI={10.1126/science.2255914}, number={4986}, journal={Science}, publisher={American Association for the Advancement of Science (AAAS)}, author={Aplan, Peter D. and Lombardi, Donald P. and Ginsberg, Ann M. and Cossman, Jeffrey and Bertness, Virginia L. and Kirsch, Ilan R.}, year={1990}, month=dec, pages={1426–1429} }