Publication Date:
1990-12-07
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aplan, P D -- Lombardi, D P -- Ginsberg, A M -- Cossman, J -- Bertness, V L -- Kirsch, I R -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1426-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute-Navy Medical Oncology Branch, Naval Hospital, Bethesda, MD 20889-5105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255914" target="_blank"〉PubMed〈/a〉
Keywords:
Base Sequence
;
Basic Helix-Loop-Helix Transcription Factors
;
Cell Line
;
Chromosome Deletion
;
DNA Nucleotidyltransferases/*metabolism
;
DNA-Binding Proteins/genetics
;
Exons
;
*Gene Rearrangement
;
Humans
;
Molecular Sequence Data
;
Oligonucleotide Probes
;
Plasmids
;
Proto-Oncogene Proteins/genetics
;
Restriction Mapping
;
Sequence Homology, Nucleic Acid
;
T-Lymphocytes
;
Transcription Factors/*genetics
;
VDJ Recombinases
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
