ArticleAmerican journal of human genetics1993
Expression cloning of multiple human cDNAs that complement the phenotypic defects of ataxia-telangiectasia group D fibroblasts.
Article in American journal of human genetics, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 68 citations in OpenAlex.
- DEK-nucleosome structure shows DEK modulates H3K27me3 and stem cell fate.Nature structural & molecular biology · 2025Article
- Super-resolution microscopy reveals the nanoscale cluster architecture of the DEK protein cancer biomarker.iScience · 2023Article
- Novel molecular mechanisms in Alzheimer's disease: The potential role of DEK in disease pathogenesis.Frontiers in aging neuroscience · 2022Review
- Loss of DEK induces radioresistance of murine restricted hematopoietic progenitors.Experimental hematology · 2018Article
- An innovative strategy to clone positive modifier genes of defects caused by mtDNA mutations: MRPS18C as suppressor gene of m.3946G>A mutation in MT-ND1 gene.Human genetics · 2017Article
- DEK is required for homologous recombination repair of DNA breaks.Scientific reports · 2017Article
- Review
- Dissecting the Potential Interplay of DEK Functions in Inflammation and Cancer.Journal of oncology · 2015Review
- Stacking the DEK: from chromatin topology to cancer stem cells.Cell cycle (Georgetown, Tex.) · 2013Review
- The human DEK oncogene regulates DNA damage response signaling and repair.Nucleic acids research · 2011Article
- Functional genomic screens identify CINP as a genome maintenance protein.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Serum from mice immunized in the context of Treg inhibition identifies DEK as a neuroblastoma tumor antigen.BMC immunology · 2007Article
- Solution NMR structure of the C-terminal domain of the human protein DEK.Protein science : a publication of the Protein Society · 2004Article
- Phosphorylation by protein kinase CK2 changes the DNA binding properties of the human chromatin protein DEK.Molecular and cellular biology · 2004Article
- Structure-specific binding of the proto-oncogene protein DEK to DNA.Nucleic acids research · 2003Article
- Transcriptional activation by AP-2alpha is modulated by the oncogene DEK.Nucleic acids research · 2003Article
- YY1 and NF-Y binding sites regulate the transcriptional activity of the dek and dek-can promoter.Oncogene · 2002Article
- Phosphorylation of serines 635 and 645 of human Rad17 is cell cycle regulated and is required for G(1)/S checkpoint activation in response to DNA damage.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
- The ATM protein is required for sustained activation of NF-kappaB following DNA damage.Oncogene · 1999Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ataxia-telangiectasia (A-T) is an inherited human disease of unknown etiology associated with neurologic degeneration, immune dysfunction, cancer risk, and genetic instability. A-T cells are sensitive to ionizing radiation and radiomimetic drugs, offering the possibility of cloning A-T genes by phenotypic complementation. We have used this sensitivity to isolate the first human cDNAs reported to complement A-T cells in culture. Complementation group D A-T fibroblasts were transfected with an episomal vector-based human cDNA library, approximately 610,000 resultant transformants were treated with the radiomimetic drug streptonigrin-resistant, and nine unrelated cDNAs were recovered from 29 surviving streptonigrin-resistant clones. Five cDNAs were mapped, but none localized to 11q23, the site of A-T complementation group A and C loci. Four of the mapped cDNAs conferred mutagen resistance to A-T D fibroblasts on secondary transfection. One cDNA was identified as a fragment of dek, a gene involved in acute myeloid leukemia. The dek cDNA fragment and pCAT4.5, a 4.5-kb cDNA that mapped to 17p11, independently complemented three different phenotypic abnormalities of A-T D fibroblasts (mutagen sensitivity, hyper-recombination, and radio-resistant DNA synthesis). The pCAT4.5 cDNA did not complement the mutagen sensitivity of an A-T group C fibroblast line, suggesting that it represents a candidate disease gene for group D A-T. Our results indicate that phenotypic complementation alone is insufficient evidence to prove that a candidate cDNA is an A-T disease gene. The complementing cDNAs may represent previously uncharacterized genes that function in the same pathway as does the A-T gene product(s) in the regulation of cellular responses to DNA damage.
Indexed as
Identifiers
7504406PMC1682482W346292765What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.