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Human RAG2 , like RAGI , is on chromosome II band p13 and therefore not linked to ataxia telangiectasia complementation groups
Author(s) -
Sherrington P. D.,
Forster A.,
Seawright A.,
Van Heyningen V.,
Rabbitts T. H.
Publication year - 1992
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.2870050417
Subject(s) - ataxia telangiectasia , genetics , recombinase , biology , locus (genetics) , complementation , recombination activating gene , gene , immunodeficiency , recombination , phenotype , dna , immune system , dna damage
Abstract Ataxia telangiectasia (A‐T) is an inherited, recessive, cancer‐prone disease with associated immunodeficiency and chromosome abnormalities involving TCR loci. The latter phenomena implicate errors of the enzyme(s) responsible for assembly of antigen receptor genes (recombinase) in disease pathogenesis. Here we report the location of a human recombination activating gene (RAG2) , in addition to RAGI , on chromosome 11, band p13, thereby formally demonstrating linkage of these genes in humans and showing that they are not linked to the known locus responsible for the A‐T syndrome. © 1992 Wiley‐Liss, Inc.