ArticleProceedings of the National Academy of Sciences of the United States of America1997
Overexpression of a truncated human topoisomerase III partially corrects multiple aspects of the ataxia-telangiectasia phenotype.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 35 citations in OpenAlex.
- Genes in a refined Smith-Magenis syndrome critical deletion interval on chromosome 17p11.2 and the syntenic region of the mouse.Genome research · 2002Article
- Topoisomerase III acts upstream of Rad53p in the S-phase DNA damage checkpoint.Molecular and cellular biology · 2001Article
- ATM-dependent expression of the insulin-like growth factor-I receptor in a pathway regulating radiation response.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- The yeast TEL1 gene partially substitutes for human ATM in suppressing hyperrecombination, radiation-induced apoptosis and telomere shortening in A-T cells.Molecular biology of the cell · 2000Article
- Expression of topoisomerase IIIalpha in normal and neoplastic tissues determined by immunohistochemistry using a novel monoclonal antibody.British journal of cancer · 2000Article
- The ATM protein is required for sustained activation of NF-kappaB following DNA damage.Oncogene · 1999Article
- The essential role of yeast topoisomerase III in meiosis depends on recombination.The EMBO journal · 1999Article
- Mammalian DNA topoisomerase IIIalpha is essential in early embryogenesis.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
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Authors and funding
4 authors at 3 institutions in 1 country.
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Abstract
Ataxia-telangiectasia (A-T) is a recessive human disease characterized by radiation sensitivity, genetic instability, immunodeficiency, and high cancer risk. We previously used expression cloning to identify CAT4.5, a human cDNA that partially suppresses multiple aspects of the A-T phenotype upon transfection into cultured cells. Sequencing CAT4.5 revealed a 1.1-kb intronic fragment followed by a related ORF of 2.5 kb that encodes the near full-length ORF for hTOP3, the first mammalian topoisomerase III to be identified. Endogenous expression of hTOP3 was found in all human tissues tested. Both pCAT4.5 and an antisense hTOP3 construct were able to inhibit spontaneous and radiation-induced apoptosis in A-T fibroblasts, whereas overexpression of a full-length hTOP3 cDNA did not. We postulate that topoisomerase III may be deregulated in A-T cells and that CAT4.5 complements the A-T phenotype via a dominant-negative mechanism. Furthermore, functional correction of hyper-recombination in A-T cells by CAT4.5 supports the hypothesis that the hTOP3 topoisomerase is involved in the control of genomic stability, perhaps in concert with the Bloom or Werner syndrome DNA helicases.
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