ArticleProceedings of the National Academy of Sciences of the United States of America1995
The product of the ataxia-telangiectasia group D complementing gene, ATDC, interacts with a protein kinase C substrate and inhibitor.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 51 citations in OpenAlex.
- TRIM29 promotes bladder cancer invasion by regulating the intermediate filament network and focal adhesion.Oncogene · 2025Article
- TRIM-endous functional network of tripartite motif 29 (TRIM29) in cancer progression and beyond.Cancer metastasis reviews · 2024Review
- ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase.The Journal of biological chemistry · 2015Article
- TRIM29 regulates the assembly of DNA repair proteins into damaged chromatin.Nature communications · 2015Article
- Up-regulation of tripartite motif-containing 29 promotes cancer cell proliferation and predicts poor survival in colorectal cancer.Medical oncology (Northwood, London, England) · 2013Article
- Ataxia-telangiectasia group D complementing gene (ATDC) upregulates matrix metalloproteinase 9 (MMP-9) to promote lung cancer cell invasion by activating ERK and JNK pathways.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Ataxia-telangiectasia group D complementing gene (ATDC) promotes lung cancer cell proliferation by activating NF-κB pathway.PloS one · 2013Article
- TRIM proteins and cancer.Nature reviews. Cancer · 2011Article
- The ATDC (TRIM29) protein binds p53 and antagonizes p53-mediated functions.Molecular and cellular biology · 2010Article
- Article
- Hint1 is a haplo-insufficient tumor suppressor in mice.Oncogene · 2006Article
- Deletion of histidine triad nucleotide-binding protein 1/PKC-interacting protein in mice enhances cell growth and carcinogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Stability of a PKCI-1-related mRNA is controlled by the splicing factor ASF/SF2: a novel function for SR proteins.Genes & development · 2002Article
- Wpkci, encoding an altered form of PKCI, is conserved widely on the avian W chromosome and expressed in early female embryos: implication of its role in female sex determination.Molecular biology of the cell · 2000Article
- HIT family genes: FHIT but not PKCI-1/HINT produces altered transcripts in colorectal cancer.British journal of cancer · 1999Article
- The histidine triad superfamily of nucleotide-binding proteins.Journal of cellular physiology · 1999Review
- Isolation, cloning and characterization of a low-molecular-mass purine nucleoside- and nucleotide-binding protein.The Biochemical journal · 1997Article
- Crystal structures of HINT demonstrate that histidine triad proteins are GalT-related nucleotide-binding proteins.Nature structural biology · 1997Article
- Three-dimensional structure of human protein kinase C interacting protein 1, a member of the HIT family of proteins.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ataxia-telangiectasia (AT) is an autosomal recessive human genetic disease characterized by immunological, neurological, and developmental defects and an increased risk of cancer. Cells from individuals with AT show sensitivity to ionizing radiation, elevated recombination, cell cycle abnormalities, and aberrant cytoskeletal organization. The molecular basis of the defect is unknown. A candidate AT gene (ATDC) was isolated on the basis of its ability to complement the ionizing radiation sensitivity of AT group D fibroblasts. Whether ATDC is mutated in any AT patients is not known. We have found that the ATDC protein physically interacts with the intermediate-filament protein vimentin, which is a protein kinase C substrate and colocalizing protein, and with an inhibitor of protein kinase C, hPKCI-1. Indirect immunofluorescence analysis of cultured cells transfected with a plasmid encoding an epitope-tagged ATDC protein localizes the protein to vimentin filaments. We suggest that the ATDC and hPKCI-1 proteins may be components of a signal transduction pathway that is induced by ionizing radiation and mediated by protein kinase C.
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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.