Publisher: International Society of Vitamins and Related Biofactors; International Union of Biochemistry and Molecular Biology, Wiley

Journal description

BioFactors is an international journal aimed at identifying and increasing our understanding of the precise biochemical effects and roles of the large number of trace substances that are required by living organisms. These include vitamins and trace elements, as well as growth factors and regulatory substances made by cells themselves. The elucidation, in a particular organism or cell line, of the roles of substances active in trace quantities, is frequently applicable directly to many other forms of life. In keeping with this unified view of biochemistry, BioFactors publishes articles dealing with the identification of new substances and the elucidation of their functions at the basic biochemical level as well as those revealing novel functions of trace substances already known.

Current impact factor: 4.59

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 4.592
2013 Impact Factor 3
2012 Impact Factor 3.088
2011 Impact Factor 4.933
2010 Impact Factor 2.793
2009 Impact Factor 0.912
2008 Impact Factor 1.23
2007 Impact Factor 1.451
2006 Impact Factor 1.095
2005 Impact Factor 1.162
2004 Impact Factor 1.273
2003 Impact Factor 1.852
2002 Impact Factor 1.815
2001 Impact Factor 1.273

Impact factor over time

Impact factor

Additional details

5-year impact 4.23
Cited half-life 6.60
Immediacy index 0.68
Eigenfactor 0.01
Article influence 1.07
Website Biofactors website
Other titles BioFactors (Online)
ISSN 0951-6433
OCLC 41948746
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo for scientific, technical and medicine titles
    • 2 years embargo for humanities and social science titles
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
    • Author's pre-print may not be updated with Publisher's Version/PDF
    • Author's pre-print must acknowledge acceptance for publication
    • On a non-profit server
    • Publisher's version/PDF cannot be used
    • Publisher source must be acknowledged with citation
    • Must link to publisher version with set statement (see policy)
    • If OnlineOpen is available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 12 months
    • If OnlineOpen is not available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 6 months
    • If OnlineOpen is available, AHRC and ESRC authors, may self-archive after 24 months
    • If OnlineOpen is not available, AHRC and ESRC authors, may self-archive after 12 months
    • Reviewed 18/03/14
    • Please see former John Wiley & Sons and Blackwell Publishing policies for articles published prior to February 2007
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Kidney dysfunction is being increasingly associated with mitochondrial diseases and coenzyme Q(10) (CoQ) deficiency. The assessment of CoQ status requires the biochemical determination of CoQ in biological fluids and different cell types, but no methods have been developed as yet for the analysis of CoQ in excretory systems. The aim of this study was to standardize a new procedure for urinary CoQ determination and to establish reference values for a paediatric population. Urinary CoQ was analyzed by HPLC with electrochemical detection. Reference values (n=43) were stratified into two age groups (2-10 years: range 24-109 nmol CoQ/gram of pellet protein; 11-17 years: range 43-139 nmol CoQ/gram of pellet protein). In conclusion, urinary CoQ analysis is a noninvasive, reliable, and reproducible method to determine urinary tract CoQ status. (c) 2015 BioFactors, 41(6):424-430, 2015
    No preview · Article · Nov 2015 · BioFactors
  • [Show abstract] [Hide abstract]
    ABSTRACT: The role of the transcription factor CCATT/enhancer binding protein alpha (C/EBPalpha) as a lineage instructive determinant in myelopoiesis is widely accepted. Furthermore, early mutational events ultimately leading to acute myeloid leukemia (AML) often involve abrogation of C/EBPalpha expression and/or function. The main focus of this review is the progression from a preclinical state to AML, and which preleukemic cell population(s) might-in general and in particular in patients with CEBPA mutations-be a target for the secondary genetic and epigenetic events leading to this progression.
    No preview · Article · May 2009 · BioFactors
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although apolipoprotein E (apoE) is the most common genetic risk factor for Alzheimer's Disease (AD), how apoE participates in AD pathogenesis remains incompletely understood. ApoE is also the major carrier of lipids in the brain. Here, we review studies showing that the lipidation status of apoE influences the metabolism of Abeta peptides, which accumulate as amyloid deposits in the neural parenchyma and cerebrovasculature. One effect of apoE is to inhibit the transport of Abeta across the blood-brain-barrier (BBB), particularly when apoE is lipidated. A second effect is to facilitate the proteolytic degradation of Abeta by neprilysin and insulin degrading enzyme (IDE), which is enhanced when apoE is lipidated. We also describe how apoE becomes lipidated and how this impacts Abeta metabolism. Specifically, genetic loss of the cholesterol transporter ABCA1 impairs apoE lipidation and promotes amyloid deposition in AD mouse models. ABCA1 catalyses the ATP-dependent transport of cholesterol and phospholipids from the plasma membrane to lipid-free apolipoproteins including apoE. Conversely, selective overexpression of ABCA1 increases apoE lipidation in the central nervous system (CNS) and eliminates the formation of amyloid plaques in vivo. Deficiency of Liver-X-Receptors (LXRs), transcription factors that stimulate ABCA1 and apoE expression, exacerbates AD pathogenesis in vivo, whereas treatment of AD mice with synthetic LXR agonists reduces amyloid load and improves cognitive performance. These studies provide new insights into the mechanisms by which apoE affects Abeta metabolism, and offer opportunities to develop novel therapeutic approaches to reduce the leading cause of dementia in the elderly.
    No preview · Article · May 2009 · BioFactors
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    ABSTRACT: It has been demonstrated that vitamin E deficiency from birth increases anxiety-related behavior using knockout animals with no vitamin E transfer proteins. The current study was undertaken to elucidate the effect of dietary vitamin E deficiency on anxiety-related behavior of rats in different housing conditions. Male Wistar strain rats were divided into two groups during the weaning period and fed a control or vitamin E-deficient diet. All rats were housed in groups (three rats per cage) for 3 weeks. In the fourth week, half of the rats in each dietary treatment were kept in social housing and the other half were kept in individual housing. Before sacrifice, rota-rod and elevated plus-maze (EPM) tests were performed to measure motor coordination and anxiety, respectively. The EPM test revealed that vitamin E-deficient rats spent less time in the open arms and showed more stretch-out posture than the control rats, showing that anxiety increased with dietary vitamin E deficiency. Furthermore, vitamin E deficiency-induced anxiety behavior was observed more prominent in individual housed rats than in social housed rats. On the basis of these results, we conclude that dietary vitamin E deficiency induces anxiety in rats especially under stress of social isolation.
    No preview · Article · May 2009 · BioFactors