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Vertebrate TBP-like protein (TLP/TRF2/TLF) stimulates TATA-less terminal deoxynucleotidyl transferase promoters in a transient reporter assay, and TFIIA-binding capacity of TLP is required for this function

Authors
Journal
Nucleic Acids Research
0305-1048
Publisher
Oxford University Press
Publication Date
Keywords
  • Articles
Disciplines
  • Biology

Abstract

gkm952 154..158 D154–D158 Nucleic Acids Research, 2008, Vol. 36, Database issue Published online 8 November 2007 doi:10.1093/nar/gkm952 miRBase: tools for microRNA genomics Sam Griffiths-Jones1,*, Harpreet Kaur Saini2, Stijn van Dongen2 and Anton J. Enright2 1Faculty of Life Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT and 2The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, Hinxton, UK Received September 14, 2007; Revised October 10, 2007; Accepted October 16, 2007 ABSTRACT miRBase is the central online repository for microRNA (miRNA) nomenclature, sequence data, annotation and target prediction. The current release (10.0) contains 5071 miRNA loci from 58 species, expressing 5922 distinct mature miRNA sequences: a growth of over 2000 sequences in the past 2 years. miRBase provides a range of data to facilitate studies of miRNA genomics: all miRNAs are mapped to their genomic coordinates. Clusters of miRNA sequences in the genome are highlighted, and can be defined and retrieved with any inter- miRNA distance. The overlap of miRNA sequences with annotated transcripts, both protein- and non- coding, are described. Finally, graphical views of the locations of a wide range of genomic features in model organisms allow for the first time the prediction of the likely boundaries of many miRNA primary transcripts. miRBase is available at http:// microrna.sanger.ac.uk/. INTRODUCTION MicroRNAs (miRNAs) are short RNA sequences expressed from longer transcripts encoded in animal, plant and virus genomes, and recently discovered in a single-celled eukaryote (1,2). miRNAs regulate the expression of target genes by binding to complemen- tary sites in their transcripts to cause translational repression or transcript degradation (3). Translational repression is thought to be the primary mechanism for imperfect target duplexes in animals, with transcript degradation the dominant mechanism for largely perfec

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