Frontiers in Genetics Journal Impact Factor & Information

Publisher: Frontiers

Journal description

Current impact factor: 0.00

Impact Factor Rankings

Additional details

5-year impact 0.00
Cited half-life 0.00
Immediacy index 0.00
Eigenfactor 0.00
Article influence 0.00
ISSN 1664-8021

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • On open access repositories
    • Authors retain copyright
    • Creative Commons Attribution License
    • Published source must be acknowledged
    • Publisher's version/PDF must be used for post-print
    • Set statement to accompany [This Document is Protected by copyright and was first published by Frontiers. All rights reserved. it is reproduced with permission.]
    • Articles are placed in PubMed Central immediately on behalf of authors.
    • Publisher last contacted on 04/10/2013
    • All titles are open access journals
  • Classification
    ​ green

Publications in this journal

  • Howard Donninger · Katharine Hobbing · M. L. Schmidt · Eric Walters · Laurie Rund · Larry Schook · Geoffrey J. Clark
    Frontiers in Genetics 08/2015; 6. DOI:10.3389/fgene.2015.00269
  • Frontiers in Genetics 08/2015; In press.
  • Source
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    ABSTRACT: The aging of the population represents one of the largest healthcare challenges facing the world today. The available scientific evidence shows that interventions are available now that can target fundamental "aging" processes or pathways. Sufficient economic evidence is available to argue convincingly that this approach will also save enormous sums of money which could then be deployed to solve other urgent global problems. However, as yet this scenario has barely entered the public consciousness and, far from being a point of vigorous debate, seems to be ignored by policy makers. Understanding why this lethargy exists is important given the urgent need to deal with the challenge represented by population aging. In this paper I hypothesize that one major cause of inaction is a widely held, but flawed, conceptual framework concerning the relationship between aging and disease that categorizes the former as "natural" and the latter as "abnormal." This perspective is sufficient in itself to act as a disincentive to intervention by rendering those who hold it prone to the "naturalistic fallacy" but can give rise to active hostility to biogerontology if coupled with loose and/or blurred understanding of the goals and potential of the field.
    Frontiers in Genetics 07/2015; 6:171. DOI:10.3389/fgene.2015.00171
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    ABSTRACT: Gene duplication is a recurring phenomenon in genome evolution and a major driving force in the gain of biological functions. Here, we examine the role of gene duplication in the origin and maintenance of moonlighting proteins, with special focus on functional redundancy and innovation, molecular tradeoffs, and genetic robustness. An overview of specific examples-mainly from yeast-suggests a widespread conservation of moonlighting behavior in duplicate genes after long evolutionary times. Dosage amplification and incomplete subfunctionalization appear to be prevalent in the maintenance of multifunctionality. We discuss the role of gene-expression divergence and paralog responsiveness in moonlighting proteins with overlapping biochemical properties. Future studies analyzing multifunctional genes in a more systematic and comprehensive manner will not only enable a better understanding of how this emerging class of protein behavior originates and is maintained, but also provide new insights on the mechanisms of evolution by gene duplication.
    Frontiers in Genetics 07/2015; 6:227. DOI:10.3389/fgene.2015.00227
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    ABSTRACT: Osteosarcoma is the most common type of bone cancer in children and adolescents. Impaired differentiation of osteoblast cells is a distinguishing feature of this aggressive disease. As improvements in survival outcomes have largely plateaued, better understanding of the bone differentiation program may provide new treatment approaches. The miRNA cluster miR-23a~27a~24-2, particularly miR-23a, has been shown to interact with genes important for bone development. However, global changes in gene expression associated with functional gain of this cluster have not been fully explored. To better understand the relationship between miR-23a expression and bone cell differentiation, we carried out a large-scale gene expression analysis in HOS cells. Experimental results demonstrate that over-expression of miR-23a delays differentiation in this system. Downstream bioinformatic analysis identified miR-23a target gene connexin-43 (Cx43/GJA1), a mediator of intercellular signaling critical to osteoblast development, as acutely affected by miR-23a levels. Connexin-43 is up-regulated in the course of HOS cell differentiation and is down-regulated in cells transfected with miR-23a. Analysis of gene expression data, housed at Gene Expression Omnibus, reveals that Cx43 is consistently up-regulated during osteoblast differentiation. Suppression of Cx43 mRNA by miR-23a was confirmed in vitro using a luciferase reporter assay. This work demonstrates novel interactions between microRNA expression, intercellular signaling and bone differentiation in osteosarcoma.
    Frontiers in Genetics 07/2015; 6:233. DOI:10.3389/fgene.2015.00233