Frontiers in Bioscience (Front Biosci)

Publisher: Frontiers in Bioscience

Journal description

The journal "Frontiers in Bioscience" is a modern forum for scientific communication. Data and information that are useful to investigators in any discipline in biology and medicine including biochemistry, microbiology, parasitology, virology, immunology, biotechnology, and bioinformatics will be published after they have been peer reviewed. This will include reviews and research articles in basic science and clinical science, as well as technical notes and protocols. Other materials that have not been traditionally published as peer reviewed articles will also be considered for publication. This will include, rare images,videos and sounds, and assimilated data in the form of a database on any subject in medicine. The journal will include useful search strategies of internet and databases related to biology and medicine, links to medically relevant journals and the guidelines to authors of scientific journals and as well as information regarding manufacturers' products and links to manufacturers' homepages. Other items that will be posted are book reviews, as well as a list of conferences.

Current impact factor: 3.52

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 3.523
2013 Impact Factor 4.249
2012 Impact Factor 3.286
2011 Impact Factor 3.52
2010 Impact Factor 4.048
2009 Impact Factor 3.736
2008 Impact Factor 3.308
2007 Impact Factor 2.989
2006 Impact Factor 2.771
2005 Impact Factor 2.623
2004 Impact Factor 3.226
2003 Impact Factor 3.603
2002 Impact Factor 3.063

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.20
Cited half-life 6.90
Immediacy index 0.71
Eigenfactor 0.01
Article influence 1.01
Website Frontiers in Bioscience website
ISSN 1093-4715
OCLC 216615969
Material type Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Frontiers in Bioscience

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors un-copyedited manuscript
    • Publisher's version/PDF cannot be used
    • Set statement to accompany (see policy)
    • Creative Commons Attribution License
    • If submission to PubMed Central is required authors must request in writing from publisher (see policy for details)
    • All titles are open access journals
  • Classification
    blue

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: DEAD box protein family of RNA helicases are vital players of RNA metabolism, and constitute the largest family of RNA helicases. Members of this family share nine conserved motifs including an Asp-Glu-Ala-Asp motif, giving this family its characteristic name as DEAD box RNA helicases. These conserved motifs confer RNA binding and RNA unwinding properties. Besides functioning in RNA metabolism, emerging evidences suggests several DEAD box RNA helicases to possess potential roles in regulating gene expression by acting as a transcriptional co-activator. Many of them are deregulated in cancers, and are implicated in possessing oncogenic potential. On the contrary, each of them also possesses tumor suppressive property in a context dependent manner. In this review, we discuss the mechanistic insights of gene regulation by DEAD box RNA helicases, and their significance in cancers.
    No preview · Article · Jan 2016 · Frontiers in Bioscience
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    ABSTRACT: First cloned in 2000, the human Histamine H4 Receptor (hH4R) is the last member of the histamine receptors family discovered so far, it belongs to the GPCR super-family and is involved in a wide variety of immunological and inflammatory responses. Potential hH4R antagonists are proposed to have therapeutic potential for the treatment of allergies, inflammation, asthma and colitis. So far, no hH4R ligands have been successfully introduced to the pharmaceutical market, which creates a strong demand for new selective ligands to be developed. in silico techniques and structural based modeling are likely to facilitate the achievement of this goal. In this review paper we attempt to cover the fundamental concepts of hH4R structure modeling and its implementations in drug discovery and development, especially those that have been experimentally tested and to highlight some ideas that are currently being discussed on the dynamic nature of hH4R and GPCRs, in regards to computerized techniques for 3-D structure modeling.
    No preview · Article · Jan 2016 · Frontiers in Bioscience

  • No preview · Article · Jan 2016 · Frontiers in Bioscience
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    ABSTRACT: Occurrence of guanine-rich sequences throughout the genome at specific locations like chromosomal ends (telomeres), promoters and Untranslated regions (UTR's) is very well documented. Quite recently, visualization of guanine-quadruplex in human and mammalian cells have also provided a very significant evidence for the in vivo existence of guanine-quadruplex, reconfirming their biological relevance in cellular processes like replication, transcription, recombination, etc. Guanine quadruplexes have enormous potential of exhibiting various topologies which differ, by number/ orientation of strands or loop orientations etc. Some relatively new polymorphic structures like 3+1 quadruplex, G-triplex, and Tri-G-quadruplex have also been proposed for the guanine-rich sequences. Various biochemical and biophysical techniques have been used to characterize these multistranded DNA structures. An extensive review of the mechanistic models of the already existing and newly emerging techniques is actually required, which may further facilitate our understanding about these structures. This review aims to summarize some of these techniques along with their requirements and limitations, which might further give some insights for the fine tuning of the solution and environmental conditions needed for facilitating guanine-quadruplex formation.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: The relationship between the mRNA level and the corresponding protein level of the cry1Ab/c gene is not well characterized in transgenic rice (Bt-ShanYou63). In this study, we compared cry1Ab/c mRNA and its protein expression in leaves at different growth stages in Bt-ShanYou63 rice. The results demonstrated that both cry1Ab/c mRNA and its protein levels changed at all of the growth stages. The cry1Ab/c transcript levels in the leaves were highest during the grain filling stage (3.29, cry/actin) and lowest during the seeding stage (1.06, cry/actin), and the protein levels of Cry1Ab/c was also highest at the grain filling stage (5.71 microgram x g-1 fresh weight, fw) and lowest during the seeding stage (2.08 microgram x g(-1) fw). There was a significant correlation between cry1Ab/c mRNA levels and the protein concentrations (r=0.742, p < 0.01). However, a linear relationship was not observed between cry1Ab/c mRNA levels and the protein levels, and the trend for mRNA expression levels was not consistent with the Cry1Ab/c protein levels in the same growth period in Bt-ShanYou63 rice.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Protein quality control (PQC) acts to minimize the level and toxicity of malfolded proteins in the cell. It is performed by an elaborate network of molecular chaperones and targeted protein degradation pathways. PQC monitors and maintains protein homeostasis or proteostasis in the cells. Whilst chaperones may actively promote refolding of malfolded proteins, the malfolded proteins which cannot be correctly refolded are degraded by the ubiquitin proteasome system (UPS) and the autophagic-lysosome pathway (ALP). The UPS degrades individual misfolded protein molecules, whereas the ALP removes large and less soluble protein aggregates and organelles. Emerging evidence indicates that dysregulated and inadequate PQC play an important role in the pathogenesis of not only classic conformational disease but more common forms of cardiac pathology such as cardiac pathological hypertrophy and heart failure. Nuclear factor erythroid 2-related factor 2 (Nrf2), a master transcription factor of cellular defense, appears to regulate the USP and the ALP by directly controlling the expression of UPS- and ALP- related genes. This article highlights an emerging role of Nrf2 in the regulation of intracellular PQC as well as its potential involvement in cardiac pathology.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Several mutations in factor XII have been reported in patients with factor XII deficiency. Here, we described three mutations in the F12 gene (c. 6635G more than A (p. G259E), c. 6658G more than C (p. R267G) and c. 8489G more than A (p. E521K)) of five patients with congenital FXII deficiency. Among these, two were heterozygous mutations. All five patients had prolonged activated partial thromboplastin time, as well as markedly decreased FXII activity and antigen levels. In vitro studies in transiently transfected HEK 293T cells demonstrated that these mutations significantly lowered the FXII levels in the culture media, but had no impact on transcription. Further protein degradation inhibition experiments with various inhibitors suggested that the three mutants were degraded intracellularly through the proteasome pathway in the pre-Golgi compartment. Moreover, G259E and R267G mutations exhibited dominant negative effects, consistent with the phenotypes observed in the heterozygous carriers. Such dominant negative effects were not due to the dimerization of FXII. Our findings suggest that the three mutations in the F12 gene are the causing reasons for the cross-reactive material-negative FXII deficiencies.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Pancreatic cancer is a devastating disease with proclivity for early metastasis, which accounts for its poor prognosis. The clinical problem of pancreatic cancer is its resistance to conventional therapies, such as chemotherapy or radiation. Based upon these challenges, the focus of research on pancreatic cancer has shifted gradually towards the tumor microenvironment. The cancer microenvironment consists of various components, including fibroblasts, endothelial cells, immune cells, and endocrine cells, that interact with each other, and with the cancer cells in a complex fashion. Evidence is accumulating that the cancer microenvironment plays an active role in disease progression, and efforts are being made to target this interplay between cancer cells and host cells, to improve the prognosis of the disease. In the present review, we describe the cellular microenvironment of pancreatic ductal adenocarcinoma (PDA), the major type of pancreatic cancer. Our hope is that a better understanding of the cellular microenvironment of PDA will eventually lead to better treatments for this disease.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Treatments for anti-N-methyl-D-aspartate (NMDA) receptor encephalitis include immunotherapy with steroids, intravenous immunoglobulin, plasma exchange, or plasmapheresis as first-line treatments, immunotherapy with rituximab or cyclophosphamide as second-line treatments, and tumor removal. In this systematic review, we evaluated previous studies and examined the association between certain microRNAs and anti-NMDA receptor encephalitis to investigate the performance of different treatment combinations. The efficacies of different combinations of treatments classified into the following four categories were compared: (I) intravenous immunoglobulin administration, (II) plasmapheresis or plasma exchange, (III) treatment with rituximab or cyclophosphamide and (IV) tumor removal. Statistical analyses showed that treatment combinations including at least two of these categories resulted in higher efficacy rates than treatment with a single form of therapy. These findings suggest that if a patient is not recovering, converting to other therapies is more likely to result in early recovery than continuing on the original therapy.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Ca(2+)/calmodulin-dependent calcineurin (CaN) plays an important role in various Ca(+2) signaling pathways, among which are those involved in cardiac diseases. It has also been shown that a heightened sympathetic tone accelerates the development of heart failure. The present study investigates whether the CaN-mediated nuclear factor of activated T-cells (NFAT) pathway is involved in cultured neonatal rat cardiac fibroblast proliferation induced by phenylephrine. CF proliferation was assessed by a cell survival assay and cell counts. Green fluorescent protein-tagged NFAT3 was used to determine the cellular location of NFAT3. CaN activity and protein levels were also determined by an activity assay kit and Western blotting, respectively. Results showed that phenylephrine promoted CF proliferation, which was abolished by α1-adrenergic receptor antagonist (prazosin), a blocker of Ca(+2) influx (nifedipine), an intracellular Ca(2+) buffer (BAPTA-AM), CaN inhibitors (cyclosporin A and FK506), and over-expression of dominant negative CaN. Phenylephrine activated CaN and evoked NFAT3 nuclear translocation, both of which were blocked by cyclosporine A (CsA) or over-expression of dominant negative CaN. These results suggest that the Ca(2+)/CaN/NFAT pathway mediates PE-induced CF proliferation, and this pathway might be a possible therapeutic target in cardiac fibrosis.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Optogenetics has taken biomedical research by storm. The power and precision at which light-gated ion channels control cellular excitability in diverse biological systems has convinced researchers of an optical future. Growing interest in optical methods has sparked the development of multiple new optogenetic tools, which allow precise control of numerous cellular processes. Among these new tools are the light-activatable G-protein coupled receptors (GPCRs) or Opto-GPCRs. The extent of the GPCR family, which in humans alone encompasses approximately 800 different proteins, and the immense therapeutic potential of Opto-GPCRs predict a big future for this juvenile field. Here the different approaches taken to design Opto-GPCRs are reviewed, outlining the advantages and disadvantages of each method for physiological and potential clinical application.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Matrix metalloproteinases (MMPs) are a family of zinc dependent endopeptidases whose main function is to degrade and deposit structural proteins within the extracellular matrix (ECM). A dysregulation of MMPs is linked to vascular diseases. MMPs are classified into collagenases, gelatinases, membrane-type, metalloelastase, stromelysins, matrilysins, enamelysins, and unclassified subgroups. The production of MMPs is stimulated by factors such as oxidative stress, growth factors and inflammation which lead to its up- or down-regulation with subsequent ECM remodeling. Normally, excess activation of MMPs is controlled by their endogenous inhibitors, tissue inhibitors of metalloproteinases (TIMPs). An imbalance of MMPs and TIMPs has been implicated in hypertension, atherosclerotic plaque formation and instability, aortic aneurysms and varicose vein wall remodeling. Also, recent evidence suggests epigenetic regulation of some MMPs in angiogenesis and atherosclerosis. Over the years, pharmacological inhibitors of MMPs have been used to modify or prevent the development of the disease with some success. In this review, we discuss recent advances in MMP biology, and their involvement in the manifestation of vascular disease.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Neutrophil granulocyte leukocytes (neutrophils) play fundamental role in the innate immune response. In the presence of adequate stimuli, neutrophils release excessive amount of reactive oxygen species (ROS) that may induce cell and tissue injury. Oxidative burst of neutrophils acts as a double-edged sword. It may contribute to the pathology of atherosclerosis and brain injury but is also necessary in resolving infections. Moreover, neutrophil-derived ROS may also have both a tumor promoting and tumor suppressing role. ROS have a specific activities and diffusion distance, which is related to their short lifetime. Therefore, the manner in which ROS will act depends on the cells targeted and the intra- and extracellular levels of individual ROS, which can further cause production of reactive aldehydes like 4-hydroxynonenal (HNE) that act as a second messengers of ROS. In this review we discuss the influence of neutrophil mediated extracellular redox reactions in ischemia reperfusion injury, transplant rejection and chronic diseases (atherosclerosis, inflammatory bowel diseases and cancer). At the end a brief overview of cellular mechanisms to maintain ROS homeostasis is given.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Heat shock proteins belong to a group of molecular chaperones responsible for the regulation of many intracellular processes. HSPs play a pivotal role in the survival of cells under stressful conditions. Over-expression of these proteins have been found in both healthy and a great number of cancer cells. HSPs may be involved in numerous carcinogenic and chemoresistant processes. Due to that fact, they may be referred to as diagnostic biomarkers of oncogenesis and potential targets for anticancer drugs. Thus, we decided to review the involvement of major HSPs in the most malignant childhood cancers.
    No preview · Article · Dec 2015 · Frontiers in Bioscience
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    ABSTRACT: Bowel diseases are common in human and animals and are characterized by intestinal dysfunction and injury. A well-established porcine model of intestinal injury can be induced by lipopolysaccharide (LPS), an endotoxin released from the cell wall of pathogenic bacteria. LPS affects the expression of genes associated with intestinal immune response, mucosal growth, energy metabolism, absorption, mucosal barrier function, and antiviral function. Transcriptional analysis of intestinal genes reveals that the duodenum, jejunum, ileum and colon respond to LPS challenge in a similar pattern. Moreover, the jejunum and ileum exhibit greater responses to LPS challenge than the duodenum and colon with regard to gene expression. Additionally, over 85% of genes are co-expressed along the small and large intestines and there is a clear distinction in gene expression patterns amongst the different intestinal segments in pigs. These findings have important implications for underlying molecular mechanisms responsible for endotoxin-induced intestinal injury and dysfunction.
    No preview · Article · Dec 2015 · Frontiers in Bioscience