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.
MeSH terms
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Base Sequence
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Basic Helix-Loop-Helix Transcription Factors
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Cell Line
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Chromosome Deletion
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DNA Nucleotidyltransferases / metabolism*
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DNA-Binding Proteins / genetics
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Exons
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Gene Rearrangement*
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Humans
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Molecular Sequence Data
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Oligonucleotide Probes
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Plasmids
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Proto-Oncogene Proteins / genetics
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Restriction Mapping
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Sequence Homology, Nucleic Acid
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T-Cell Acute Lymphocytic Leukemia Protein 1
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T-Lymphocytes
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Transcription Factors / genetics*
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VDJ Recombinases
Substances
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Basic Helix-Loop-Helix Transcription Factors
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DNA-Binding Proteins
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Oligonucleotide Probes
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Proto-Oncogene Proteins
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T-Cell Acute Lymphocytic Leukemia Protein 1
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Transcription Factors
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TAL1 protein, human
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DNA Nucleotidyltransferases
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VDJ Recombinases