Nucleic Acids Research (NUCLEIC ACIDS RES)

Publisher: Oxford University Press (OUP)

Journal description

Nucleic Acids Research (NAR) publishes the results of leading edge research into physical, chemical, biochemical and biological aspects of nucleic acids and proteins involved in nucleic acid metabolism and/or interactions. It enables the rapid publication of papers under the following categories: RNA, molecular biology, chemistry, genomics, computational biology and structural biology. A Survey and Summary section provides a format for brief reviews. The first issue of each year is devoted to biological databases.

Current impact factor: 9.11

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 9.112
2013 Impact Factor 8.808
2012 Impact Factor 8.278
2011 Impact Factor 8.026
2010 Impact Factor 7.836
2009 Impact Factor 7.479
2008 Impact Factor 6.878
2007 Impact Factor 6.954
2006 Impact Factor 6.317
2005 Impact Factor 7.552
2004 Impact Factor 7.26
2003 Impact Factor 6.575
2002 Impact Factor 7.051
2001 Impact Factor 6.373
2000 Impact Factor 5.396
1999 Impact Factor 5.748
1998 Impact Factor 4.878
1997 Impact Factor 4.188
1996 Impact Factor 4.488
1995 Impact Factor 4.235
1994 Impact Factor 4.097
1993 Impact Factor 3.783
1992 Impact Factor 3.294

Impact factor over time

Impact factor

Additional details

5-year impact 8.87
Cited half-life 7.40
Immediacy index 2.33
Eigenfactor 0.34
Article influence 3.49
Website Nucleic Acids Research website
Other titles Nucleic acids research
ISSN 0305-1048
OCLC 1791693
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Oxford University Press (OUP)

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • Creative Commons Attribution License or Creative Commons Attribution Non-Commercial License available
    • Pre-print on author's personal website, employers website or subject repository
    • Pre-print can only be posted prior to acceptance
    • Pre-print must be accompanied by set statement (see link)
    • Pre-print must not be replaced with post-print, instead a link to published version with amended set statement should be made
    • Publisher's version/PDF must be used
    • Publisher's version/PDF on institutional repository or centrally organised repositories
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany archived copy (see policy)
    • Eligible authors may deposit in OpenDepot
    • Publisher will deposit on behalf of NIH, HHMI, UK MRC, Telethon and Wellcome Trust funded authors to PubMed Central and Europe PMC
    • All titles are open access journals
    • This policy is an exception to the default policies of 'Oxford University Press (OUP)'
  • Classification

Publications in this journal

  • Jian-Rong Li · Chuan-Hu Sun · Wenyuan Li · Rou-Fang Chao · Chieh-Chen Huang · Xianghong Jasmine Zhou · Chun-Chi Liu ·

    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1282
  • Nir Atias · Martin Kupiec · Roded Sharan ·

    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1284
  • Alexey Moskalev · Svetlana Zhikrivetskaya · Mikhail Shaposhnikov · Evgenia Dobrovolskaya · Roman Gurinovich · Oleg Kuryan · Aleksandr Pashuk · Leslie C. Jellen · Alex Aliper · Alex Peregudov · Alex Zhavoronkov ·

    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1287
  • Guangshun Wang · Xia Li · Zhe Wang ·

    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1278
  • Julie Neubauer · Minako Ogino · Todd J. Green · Tomoaki Ogino ·

    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1286
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    ABSTRACT: Cyclic di- and linear oligo-nucleotide signals activate defenses against invasive nucleic acids in animal immunity; however, their evolutionary antecedents are poorly understood. Using comparative genomics, sequence and structure analysis, we uncovered a vast network of systems defined by conserved prokaryotic gene-neighborhoods, which encode enzymes generating such nucleotides or alternatively processing them to yield potential signaling molecules. The nucleotide-generating enzymes include several clades of the DNA-polymerase β-like superfamily (including Vibrio cholerae DncV), a minimal version of the CRISPR polymerase and DisA-like cyclic-di-AMP synthetases. Nucleotide-binding/processing domains include TIR domains and members of a superfamily prototyped by Smf/DprA proteins and base (cytokinin)-releasing LOG enzymes. They are combined in conserved gene-neighborhoods with genes for a plethora of protein superfamilies, which we predict to function as nucleotide-sensors and effectors targeting nucleic acids, proteins or membranes (pore-forming agents). These systems are sometimes combined with other biological conflict-systems such as restriction-modification and CRISPR/Cas. Interestingly, several are coupled in mutually exclusive neighborhoods with either a prokaryotic ubiquitin-system or a HORMA domain-PCH2-like AAA+ ATPase dyad. The latter are potential precursors of equivalent proteins in eukaryotic chromosome dynamics. Further, components from these nucleotide-centric systems have been utilized in several other systems including a novel diversity-generating system with a reverse transcriptase. We also found the Smf/DprA/LOG domain from these systems to be recruited as a predicted nucleotide-binding domain in eukaryotic TRPM channels. These findings point to evolutionary and mechanistic links, which bring together CRISPR/Cas, animal interferon-induced immunity, and several other systems that combine nucleic-acid-sensing and nucleotide-dependent signaling.
    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1267
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    ABSTRACT: Lynx ( is a web-based database and a knowledge extraction engine. It supports annotation and analysis of high-throughput experimental data and generation of weighted hypotheses regarding genes and molecular mechanisms contributing to human phenotypes or conditions of interest. Since the last release, the Lynx knowledge base (LynxKB) has been periodically updated with the latest versions of the existing databases and supplemented with additional information from public databases. These additions have enriched the data annotations provided by Lynx and improved the performance of Lynx analytical tools. Moreover, the Lynx analytical workbench has been supplemented with new tools for reconstruction of co-expression networks and feature-and-network-based prioritization of genetic factors and molecular mechanisms. These developments facilitate the extraction of meaningful knowledge from experimental data and LynxKB. The Service Oriented Architecture provides public access to LynxKB and its analytical tools via user-friendly web services and interfaces.
    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1257

  • Nucleic Acids Research 11/2015;
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    ABSTRACT: Interactions between proteins and small molecules are an integral part of biological processes in living organisms. Information on these interactions is dispersed over many databases, texts and prediction methods, which makes it difficult to get a comprehensive overview of the available evidence. To address this, we have developed STITCH ('Search Tool for Interacting Chemicals') that integrates these disparate data sources for 430 000 chemicals into a single, easy-to-use resource. In addition to the increased scope of the database, we have implemented a new network view that gives the user the ability to view binding affinities of chemicals in the interaction network. This enables the user to get a quick overview of the potential effects of the chemical on its interaction partners. For each organism, STITCH provides a global network; however, not all proteins have the same pattern of spatial expression. Therefore, only a certain subset of interactions can occur simultaneously. In the new, fifth release of STITCH, we have implemented functionality to filter out the proteins and chemicals not associated with a given tissue. The STITCH database can be downloaded in full, accessed programmatically via an extensive API, or searched via a redesigned web interface at
    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1277
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    ABSTRACT: Small non-coding RNAs (e.g. miRNAs) and long non-coding RNAs (e.g. lincRNAs and circRNAs) are emerging as key regulators of various cellular processes. However, only a very small fraction of these enigmatic RNAs have been well functionally characterized. In this study, we describe deepBase v2.0 (, an updated platform, to decode evolution, expression patterns and functions of diverse ncRNAs across 19 species. deepBase v2.0 has been updated to provide the most comprehensive collection of ncRNA-derived small RNAs generated from 588 sRNA-Seq datasets. Moreover, we developed a pipeline named lncSeeker to identify 176 680 high-confidence lncRNAs from 14 species. Temporal and spatial expression patterns of various ncRNAs were profiled. We identified approximately 24 280 primate-specific, 5193 rodent-specific lncRNAs, and 55 highly conserved lncRNA orthologs between human and zebrafish. We annotated 14 867 human circRNAs, 1260 of which are orthologous to mouse circRNAs. By combining expression profiles and functional genomic annotations, we developed lncFunction web-server to predict the function of lncRNAs based on protein-lncRNA co-expression networks. This study is expected to provide considerable resources to facilitate future experimental studies and to uncover ncRNA functions.
    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1273
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    ABSTRACT: The MutationAligner web resource, available at, enables discovery and exploration of somatic mutation hotspots identified in protein domains in currently (mid-2015) more than 5000 cancer patient samples across 22 different tumor types. Using multiple sequence alignments of protein domains in the human genome, we extend the principle of recurrence analysis by aggregating mutations in homologous positions across sets of paralogous genes. Protein domain analysis enhances the statistical power to detect cancer-relevant mutations and links mutations to the specific biological functions encoded in domains. We illustrate how the MutationAligner database and interactive web tool can be used to explore, visualize and analyze mutation hotspots in protein domains across genes and tumor types. We believe that MutationAligner will be an important resource for the cancer research community by providing detailed clues for the functional importance of particular mutations, as well as for the design of functional genomics experiments and for decision support in precision medicine. MutationAligner is slated to be periodically updated to incorporate additional analyses and new data from cancer genomics projects.
    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1132
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    ABSTRACT: Mitochondria are the only organelles in the animal cells that have their own genome. Due to a key role in energy production, generation of damaging factors (ROS, heat), and apoptosis, mitochondria and mtDNA in particular have long been considered one of the major players in the mechanisms of aging, longevity and age-related diseases. The rapidly increasing number of species with fully sequenced mtDNA, together with accumulated data on longevity records, provides a new fascinating basis for comparative analysis of the links between mtDNA features and animal longevity. To facilitate such analyses and to support the scientific community in carrying these out, we developed the MitoAge database containing calculated mtDNA compositional features of the entire mitochondrial genome, mtDNA coding (tRNA, rRNA, protein-coding genes) and non-coding (D-loop) regions, and codon usage/amino acids frequency for each protein-coding gene. MitoAge includes 922 species with fully sequenced mtDNA and maximum lifespan records. The database is available through the MitoAge website ( or, which provides the necessary tools for searching, browsing, comparing and downloading the data sets of interest for selected taxonomic groups across the Kingdom Animalia. The MitoAge website assists in statistical analysis of different features of the mtDNA and their correlative links to longevity.
    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1187
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    ABSTRACT: Although defective repair of DNA double-strand breaks (DSBs) leads to neurodegenerative diseases, the processes underlying their production and signaling in non-replicating cells are largely unknown. Stabilized topoisomerase I cleavage complexes (Top1cc) by natural compounds or common DNA alterations are transcription-blocking lesions whose repair depends primarily on Top1 proteolysis and excision by tyrosyl-DNA phosphodiesterase-1 (TDP1). We previously reported that stabilized Top1cc produce transcription-dependent DSBs that activate ATM in neurons. Here, we use camptothecin (CPT)-treated serum-starved quiescent cells to induce transcription-blocking Top1cc and show that those DSBs are generated during Top1cc repair from Top1 peptide-linked DNA single-strand breaks generated after Top1 proteolysis and before excision by TDP1. Following DSB induction, ATM activates DNA-PK whose inhibition suppresses H2AX and H2A ubiquitination and the later assembly of activated ATM into nuclear foci. Inhibition of DNA-PK also reduces Top1 ubiquitination and proteolysis as well as resumption of RNA synthesis suggesting that DSB signaling further enhances Top1cc repair. Finally, we show that co-transcriptional DSBs kill quiescent cells. Together, these new findings reveal that DSB production and signaling by transcription-blocking Top1 lesions impact on non-replicating cell fate and provide insights on the molecular pathogenesis of neurodegenerative diseases such as SCAN1 and AT syndromes, which are caused by TDP1 and ATM deficiency, respectively.
    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1196
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    ABSTRACT: During mitosis the chromatin undergoes dramatic architectural changes with the halting of the transcriptional processes and evacuation of nearly all transcription associated machinery from genes and promoters. Molecular bookmarking of genes during mitosis is a mechanism of faithfully transmitting cell-specific transcription patterns through cell division. We previously discovered chromatin ubiquitination at active promoters as a potential mitotic bookmark. In this study, we identify the enzymes involved in the deposition of ubiquitin before mitosis. We find that the polycomb complex proteins BMI1 and RING1A regulate the ubiquitination of chromatin associated proteins bound to promoters, and this modification is necessary for the expression of marked genes once the cells enter G1. Depletion of RING1A, and thus inactivation of mitotic bookmarking by ubiquitination, is deleterious to progression through G1, cell survival and proliferation. Though the polycomb complex proteins are thought to primarily regulate gene expression by transcriptional repression, in this study, we discover that these two polycomb proteins regulate the transcription of active genes during the mitosis to G1 transition.
    Nucleic Acids Research 11/2015; DOI:10.1093/nar/gkv1223