ArticleProceedings of the National Academy of Sciences of the United States of America1991
Functional complementation of ataxia-telangiectasia group D (AT-D) cells by microcell-mediated chromosome transfer and mapping of the AT-D locus to the region 11q22-23.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- The manipulation of chromosomes by mankind: the uses of microcell-mediated chromosome transfer.Chromosoma · 2005Review
- Substantial narrowing of the Niemann-Pick C candidate interval by yeast artificial chromosome complementation.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Regulation of the cell cycle following DNA damage in normal and Ataxia telangiectasia cells.Experientia · 1996Review
- The product of the ataxia-telangiectasia group D complementing gene, ATDC, interacts with a protein kinase C substrate and inhibitor.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Human liver mitochondrial carnitine palmitoyltransferase I: characterization of its cDNA and chromosomal localization and partial analysis of the gene.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Studies on phenotypic complementation of ataxia-telangiectasia cells by chromosome transfer.American journal of human genetics · 1995Article
- Predisposition for breast cancer in carriers of constitutional translocation 11q;22q.American journal of human genetics · 1994Article
- A human gene that restores the DNA-repair defect in SCID mice is located on 8p11.1-->q11.1.Human genetics · 1994Article
- Expression cloning of multiple human cDNAs that complement the phenotypic defects of ataxia-telangiectasia group D fibroblasts.American journal of human genetics · 1993Article
- Human chromosome 11 complements ataxia-telangiectasia cells but does not complement the defect in AT-like Chinese hamster cell mutants.Human genetics · 1993Article
- Absence of linkage to the ataxia telangiectasia locus in familial breast cancer.Human genetics · 1993Article
- A family showing no evidence of linkage between the ataxia telangiectasia gene and chromosome 11q22-23.Journal of medical genetics · 1993Article
- Elevated sister chromatid exchange phenotype of Bloom syndrome cells is complemented by human chromosome 15.Proceedings of the National Academy of Sciences of the United States of America · 1992Article
- Cloning of a candidate gene for ataxia-telangiectasia group D.American journal of human genetics · 1992Article
- Ataxia telangiectasia genes and predisposition to leukaemia, lymphoma and breast cancer.British journal of cancer · 1992Review
- Correction of xeroderma pigmentosum complementation group D mutant cell phenotypes by chromosome and gene transfer: involvement of the human ERCC2 DNA repair gene.Proceedings of the National Academy of Sciences of the United States of America · 1992Article
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8 authors at 1 institution in 1 country.
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Abstract
The hereditary human disease ataxia-telangiectasia (AT) is characterized by phenotypic complexity at the cellular level. We show that multiple mutant phenotypes of immortalized AT cells from genetic complementation group D (AT-D) are corrected after the introduction of a single human chromosome from a human-mouse hybrid line by microcell-mediated chromosome transfer. This chromosome is cytogenetically abnormal. It consists primarily of human chromosome 18, but it carries translocated material from the region 11q22-23, where one or more AT genes have been previously mapped by linkage analysis. A cytogenetically normal human chromosome 18 does not complement AT-D cells after microcell-mediated transfer, whereas a normal human chromosome 11 does. We conclude that the AT-D gene is located on chromosome 11q22-23.
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