{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T17:30:48Z","timestamp":1793640648392,"version":"4.5.1"},"reference-count":32,"publisher":"National Academy of Sciences","issue":"21","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1997,10,14]]},"abstract":"<jats:p>\n                    The murine gene\n                    <jats:italic>CHD1<\/jats:italic>\n                    (\n                    <jats:italic>MmCHD1<\/jats:italic>\n                    ) was previously isolated in a search for proteins that bound a DNA promoter element. The presence of chromo (chromatin organization modifier) domains and an SNF2-related helicase\/ATPase domain led to speculation that this gene regulated chromatin structure or gene transcription. This study describes the cloning and characterization of three novel human genes related to\n                    <jats:italic>MmCHD1<\/jats:italic>\n                    . Examination of sequence databases produced several more related genes, most of which were not known to be similar to\n                    <jats:italic>MmCHD1<\/jats:italic>\n                    , yielding a total of 12 highly conserved CHD genes from organisms as diverse as yeast and mammals. The major region of sequence variation is in the C-terminal part of the protein, a region with DNA-binding activity in MmCHD1. Targeted deletion of\n                    <jats:italic>ScCHD1<\/jats:italic>\n                    , the sole\n                    <jats:italic>Saccharomyces cerevesiae<\/jats:italic>\n                    CHD gene, was performed with deletion strains being less sensitive than wild type to the cytotoxic effect of 6-azauracil. This finding suggested that enhanced transcriptional arrest at RNA polymerase II pause sites due to 6-azauracil-induced nucleotide pool depletion was reduced in the deletion strain and that\n                    <jats:italic>ScCHD1<\/jats:italic>\n                    inhibited transcription. This observation, along with the known roles of other proteins with chromo or SNF2-related helicase\/ATPase domains, suggests that alteration of gene expression by CHD genes might occur by modifications of chromatin structure, with altered access of the transcriptional apparatus to its chromosomal DNA template.\n                  <\/jats:p>","DOI":"10.1073\/pnas.94.21.11472","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:32:33Z","timestamp":1027679553000},"page":"11472-11477","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":326,"title":["Characterization of the CHD family of\u2009proteins"],"prefix":"10.1073","volume":"94","author":[{"given":"Trevor","family":"Woodage","sequence":"first","affiliation":[{"name":"Laboratory of Gene Transfer and Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892; and Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Munira A.","family":"Basrai","sequence":"additional","affiliation":[{"name":"Laboratory of Gene Transfer and Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892; and Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas D.","family":"Baxevanis","sequence":"additional","affiliation":[{"name":"Laboratory of Gene Transfer and Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892; and Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip","family":"Hieter","sequence":"additional","affiliation":[{"name":"Laboratory of Gene Transfer and Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892; and Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francis S.","family":"Collins","sequence":"additional","affiliation":[{"name":"Laboratory of Gene Transfer and Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892; and Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[1997,10,14]]},"reference":[{"key":"e_1_3_4_1_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.6.2414"},{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/19.4.789"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-4838(96)00165-3"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/23.14.2715"},{"key":"e_1_3_4_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81918-2"},{"key":"e_1_3_4_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.15.5.2745"},{"key":"e_1_3_4_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2836(05)80360-2"},{"key":"e_1_3_4_8_2","volume-title":"phylip Phylogeny Inference Package","author":"Felsenstein J","year":"1993","unstructured":"J Felsenstein phylip Phylogeny Inference Package (Univ. of Washington, Seattle, 1993)."},{"key":"e_1_3_4_9_2","volume-title":"Atlas of Protein Sequence and Structure","author":"Dayhoff M O","year":"1978","unstructured":"M O Dayhoff Atlas of Protein Sequence and Structure (Natl. 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