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Functionally, uORFs are implicated in downstream translational regulation of the main protein coding sequence and may serve as a source of non-canonical peptides. Genetic defects in uORF sequences have been linked to the development of various diseases, including cancer. To simplify uORF-related research, the initial release of uORFdb in 2014 provided a comprehensive and manually curated collection of uORF-related literature. Here, we present an updated sequence-based version of uORFdb, accessible at https:\/\/www.bioinformatics.uni-muenster.de\/tools\/uorfdb. The new uORFdb enables users to directly access sequence information, graphical displays, and genetic variation data for over 2.4 million human uORFs. It also includes sequence data of &amp;gt;4.2 million uORFs in 12 additional species. Multiple uORFs can be displayed in transcript- and reading-frame-specific models to visualize the translational context. A variety of filters, sequence-related information, and links to external resources (UCSC Genome Browser, dbSNP, ClinVar) facilitate immediate in-depth analysis of individual uORFs. The database also contains uORF-related somatic variation data obtained from whole-genome sequencing (WGS) analyses of 677 cancer samples collected by the TCGA consortium.<\/jats:p>","DOI":"10.1093\/nar\/gkac899","type":"journal-article","created":{"date-parts":[[2022,10,28]],"date-time":"2022-10-28T15:38:19Z","timestamp":1666971499000},"page":"D328-D336","source":"Crossref","is-referenced-by-count":36,"title":["The new uORFdb: integrating literature, sequence, and variation data in a central hub for uORF research"],"prefix":"10.1093","volume":"51","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6509-2063","authenticated-orcid":false,"given":"Felix","family":"Manske","sequence":"first","affiliation":[{"name":"Institute of Bioinformatics, University of M\u00fcnster , M\u00fcnster \u00a048149, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2739-0251","authenticated-orcid":false,"given":"Lynn","family":"Ogoniak","sequence":"additional","affiliation":[{"name":"Institute of Bioinformatics, University of M\u00fcnster , M\u00fcnster \u00a048149, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6910-8341","authenticated-orcid":false,"given":"Lara","family":"J\u00fcrgens","sequence":"additional","affiliation":[{"name":"Department of Medicine A, Hematology, Oncology, Hemostaseology and Pneumology, University Hospital M\u00fcnster , M\u00fcnster \u00a048149, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8743-2348","authenticated-orcid":false,"given":"Norbert","family":"Grundmann","sequence":"additional","affiliation":[{"name":"Institute of Bioinformatics, University of M\u00fcnster , M\u00fcnster \u00a048149, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2303-9541","authenticated-orcid":false,"given":"Wojciech","family":"Maka\u0142owski","sequence":"additional","affiliation":[{"name":"Institute of Bioinformatics, University of M\u00fcnster , M\u00fcnster \u00a048149, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1899-3261","authenticated-orcid":false,"given":"Klaus","family":"Wethmar","sequence":"additional","affiliation":[{"name":"Department of Medicine A, Hematology, Oncology, Hemostaseology and Pneumology, University Hospital M\u00fcnster , M\u00fcnster \u00a048149, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2022,10,28]]},"reference":[{"key":"2023010804332953700_B1","doi-asserted-by":"crossref","first-page":"201","DOI":"10.1016\/0092-8674(86)90384-3","article-title":"Multiple upstream AUG codons mediate translational control of GCN4","volume":"45","author":"Mueller","year":"1986","journal-title":"Cell"},{"key":"2023010804332953700_B2","first-page":"486","article-title":"Suppression of ribosomal reinitiation at upstream open reading frames in amino acid-starved cells forms the basis for GCN4 translational control","volume":"11","author":"Abastado","year":"1991","journal-title":"Mol. 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