Nature Genetics Journal Impact Factor & Information

Publisher: Nature Publishing Group

Journal description

The journal publishes advances in all fields of modern genetic research, with a special emphasis on mammalian genetics and gene function.

Current impact factor: 29.35

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 29.352
2013 Impact Factor 29.648
2012 Impact Factor 35.209
2011 Impact Factor 35.532
2010 Impact Factor 36.377
2009 Impact Factor 34.284
2008 Impact Factor 30.259
2007 Impact Factor 25.556
2006 Impact Factor 24.176
2005 Impact Factor 25.797
2004 Impact Factor 24.695
2003 Impact Factor 26.494
2002 Impact Factor 26.711
2001 Impact Factor 29.6
2000 Impact Factor 30.91
1999 Impact Factor 30.693
1998 Impact Factor 40.361
1997 Impact Factor 38.854
1996 Impact Factor 31.473
1995 Impact Factor 28.543
1994 Impact Factor 22.568
1993 Impact Factor 19.844

Impact factor over time

Impact factor

Additional details

5-year impact 32.41
Cited half-life 7.50
Immediacy index 5.94
Eigenfactor 0.26
Article influence 15.91
Website Nature Genetics website
Other titles Nature genetics, Genetics
ISSN 1061-4036
OCLC 25302333
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Author's pre-print on arXiv or bioRXiv
    • Author's post-print on author's personal website, institutional repository, PubMed Central or funding body's archive
    • Published source must be acknowledged
    • Must link to publisher version with DOI
    • Publisher's version/PDF cannot be used
  • Classification

Publications in this journal

  • Hanwen Bai · Akdes Serin Harmancı · E Zeynep Erson-Omay · Jie Li · Süleyman Coşkun · Matthias Simon · Boris Krischek · Koray Özduman · S Bülent Omay · Eric A Sorensen · [...] · Octavian Henegariu · Jennifer Moliterno · Angeliki Louvi · Timothy A Chan · Stacey L Tannheimer · M Necmettin Pamir · Alexander O Vortmeyer · Kaya Bilguvar · Katsuhito Yasuno · Murat Günel ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Gliomas represent approximately 30% of all central nervous system tumors and 80% of malignant brain tumors. To understand the molecular mechanisms underlying the malignant progression of low-grade gliomas with mutations in IDH1 (encoding isocitrate dehydrogenase 1), we studied paired tumor samples from 41 patients, comparing higher-grade, progressed samples to their lower-grade counterparts. Integrated genomic analyses, including whole-exome sequencing and copy number, gene expression and DNA methylation profiling, demonstrated nonlinear clonal expansion of the original tumors and identified oncogenic pathways driving progression. These include activation of the MYC and RTK-RAS-PI3K pathways and upregulation of the FOXM1- and E2F2-mediated cell cycle transitions, as well as epigenetic silencing of developmental transcription factor genes bound by Polycomb repressive complex 2 in human embryonic stem cells. Our results not only provide mechanistic insight into the genetic and epigenetic mechanisms driving glioma progression but also identify inhibition of the bromodomain and extraterminal (BET) family as a potential therapeutic approach.
    Nature Genetics 11/2015; DOI:10.1038/ng.3457
  • [Show abstract] [Hide abstract]
    ABSTRACT: Small nucleolar RNAs (snoRNAs) are conserved noncoding RNAs best studied as ribonucleoprotein (RNP) guides in RNA modification. To explore their role in cancer, we compared 5,473 tumor-normal genome pairs to identify snoRNAs with frequent copy number loss. The SNORD50A-SNORD50B snoRNA locus was deleted in 10-40% of 12 common cancers, where its loss was associated with reduced survival. A human protein microarray screen identified direct SNORD50A and SNORD50B RNA binding to K-Ras. Loss of SNORD50A and SNORD50B increased the amount of GTP-bound, active K-Ras and hyperactivated Ras-ERK1/ERK2 signaling. Loss of these snoRNAs also increased binding by farnesyltransferase to K-Ras and increased K-Ras prenylation, suggesting that KRAS mutation might synergize with SNORD50A and SNORD50B loss in cancer. In agreement with this hypothesis, CRISPR-mediated deletion of SNORD50A and SNORD50B in KRAS-mutant tumor cells enhanced tumorigenesis, and SNORD50A and SNORD50B deletion and oncogenic KRAS mutation co-occurred significantly in multiple human tumor types. SNORD50A and SNORD50B snoRNAs thus directly bind and inhibit K-Ras and are recurrently deleted in human cancer.
    Nature Genetics 11/2015; DOI:10.1038/ng.3452
  • [Show abstract] [Hide abstract]
    ABSTRACT: Three new studies have identified new genes and sequence variants implicated in blood lipids, inflammatory markers, hemoglobin levels and adult height variation in Sardinia. These reports highlight the usefulness of large-scale genotype imputation based on whole-genome sequencing, particularly in isolated populations, in studying the genetics of complex human phenotypes.
    Nature Genetics 11/2015; 47(11):1224-1225. DOI:10.1038/ng.3426
  • [Show abstract] [Hide abstract]
    ABSTRACT: Whole-exome sequencing has revolutionized the identification of genes with dominant disease-associated variants for rare clinically and genetically heterogeneous disorders, but the identification of genes with recessive disease-associated variants has been less successful. A new study now provides a framework integrating Mendelian variant filtering with statistical assessments of patients' genotypes and phenotypes, thereby catalyzing the discovery of novel mutations associated with recessive disease.
    Nature Genetics 10/2015; 47(11):1222-1224. DOI:10.1038/ng.3425
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pancreatic cancers consist of a heterogeneous amalgam of assorted cell types, making it challenging to develop a classification system that groups these tumors according to common molecular features. A new study tackles this important issue using bioinformatics approaches to decipher gene expression signatures derived specifically from either tumor cells or nonmalignant stromal cells that predict patient outcome and may inform personalized treatments.
    Nature Genetics 09/2015; 47(10):1102-1103. DOI:10.1038/ng.3408
  • [Show abstract] [Hide abstract]
    ABSTRACT: The three-dimensional organization of the genome has an important role in orchestrating gene expression, but its regulation is poorly understood. Now, a new study uncovers a major role for Polycomb components of the PRC1 complex in organizing physical networks of genes that are co-repressed to maintain pluripotency.
    Nature Genetics 09/2015; 47(10):1105-1106. DOI:10.1038/ng.3411
  • [Show abstract] [Hide abstract]
    ABSTRACT: Expression of the intermediate filament protein keratin 17 (K17) is robustly upregulated in inflammatory skin diseases and in many tumors originating in stratified and pseudostratified epithelia. We report that autoimmune regulator (Aire), a transcriptional regulator, is inducibly expressed in human and mouse tumor keratinocytes in a K17-dependent manner and is required for timely onset of Gli2-induced skin tumorigenesis in mice. The induction of Aire mRNA in keratinocytes depends on a functional interaction between K17 and the heterogeneous nuclear ribonucleoprotein hnRNP K. Further, K17 colocalizes with Aire protein in the nucleus of tumor-prone keratinocytes, and each factor is bound to a specific promoter region featuring an NF-κB consensus sequence in a relevant subset of K17- and Aire-dependent proinflammatory genes. These findings provide radically new insight into keratin intermediate filament and Aire function, along with a molecular basis for the K17-dependent amplification of inflammatory and immune responses in diseased epithelia.
    Nature Genetics 07/2015; 47(8). DOI:10.1038/ng.3355