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pmid: 2255914
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.
Gene Rearrangement, Base Sequence, T-Lymphocytes, Molecular Sequence Data, Restriction Mapping, Exons, Cell Line, DNA-Binding Proteins, Proto-Oncogene Proteins, Sequence Homology, Nucleic Acid, DNA Nucleotidyltransferases, Basic Helix-Loop-Helix Transcription Factors, Humans, Chromosome Deletion, Oligonucleotide Probes, VDJ Recombinases, T-Cell Acute Lymphocytic Leukemia Protein 1, Plasmids, Transcription Factors
Gene Rearrangement, Base Sequence, T-Lymphocytes, Molecular Sequence Data, Restriction Mapping, Exons, Cell Line, DNA-Binding Proteins, Proto-Oncogene Proteins, Sequence Homology, Nucleic Acid, DNA Nucleotidyltransferases, Basic Helix-Loop-Helix Transcription Factors, Humans, Chromosome Deletion, Oligonucleotide Probes, VDJ Recombinases, T-Cell Acute Lymphocytic Leukemia Protein 1, Plasmids, Transcription Factors
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