Critical Reviews in Eukaryotic Gene Expression (CRIT REV EUKAR GENE)

Publisher: Begell House

Journal description

Critical Reviews in Eukaryotic Gene Expression presents timely concepts and experimental approaches that are contributing to rapid advances in our understanding of gene regulation, organization, and structure. The journal provides in-depth critical reviews of the current literature on a well-defined topic of immediate interest, written by recognized specialists in the field. Extensive reference lists accompany all articles, providing a comprehensive information resource. The contributions of molecular, cellular, biochemical, and genetic approaches to eukaryotic gene expression are incorporated into each review. The relationship between gene structure and function is stressed, with emphasis on coordinate control of biological processes. Regulatory mechanisms are explored from the perspective of sequences and regulatory molecules that influence structure and expression of eukaryotic genes, as well as within the context of cellular architecture and its relationship to development of cell specialization and tissue organization.

Current impact factor: 2.39

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.385
2012 Impact Factor 2.065
2011 Impact Factor 3.075
2010 Impact Factor 4.111
2009 Impact Factor 2.949
2008 Impact Factor 1.947
2007 Impact Factor 2.132
2006 Impact Factor 3.342
2005 Impact Factor 2.846
2004 Impact Factor 2.359
2003 Impact Factor 2.576
2002 Impact Factor 3.103
2001 Impact Factor 3.943
2000 Impact Factor 4.383
1999 Impact Factor 4.206
1998 Impact Factor 3.833

Impact factor over time

Impact factor
Year

Additional details

5-year impact 2.78
Cited half-life 7.40
Immediacy index 0.29
Eigenfactor 0.00
Article influence 0.86
Website Critical Reviews in Eukaryotic Gene Expression website
Other titles Critical reviews in eukaryotic gene expression, Eukaryotic gene expression
ISSN 1045-4403
OCLC 20114919
Material type Periodical
Document type Journal / Magazine / Newspaper

Publisher details

Begell House

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • Deposit in institutional repositories is not allowed
    • NIH Authors can deposit in PubMed Central for public release after 12 month embargo
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Degenerated intervertebral discs (d-IVDs) contribute to low back pain (LBP) and are highly common. While some d-IVDs cause discogenic LBP, others are pain-free. Understanding the differences in pathophysiology between painful and pain-free intervertebral disc degeneration (IDD), especially the pathogenic signaling involved in the regulation of painful d-IVDs, is vital for achieving satisfactory effects in clinical treatment. In this review, we revisit recent findings on the detection of inflammatory factors in d-IVDs and summarize the differences between d-IVDs that are painful and those that are pain-free. We postulate that persistent inflammation and innervation are the key factors distinguishing those that are symptomatic and those that are not. This highlights the necessity to use painful, rather than pain-free, degenerated discs in the mechanistic study of disc degeneration and in the development of regenerative approaches, to avoid false positive/negative outcomes. Based on previous molecular d-IVD studies, we also postulate the signaling events from disc overload/ injury to discogenic pain. Although these proposed events are supported by experimental findings, many details about how they are interconnected are not addressed and therefore require experimental investigation.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(1). DOI:10.1615/CritRevEukaryotGeneExpr.2015012369
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    ABSTRACT: The success of solid-organ transplantation was made possible by recognizing that destruction of the graft is caused by an alloimmune-mediated process. For the past decade, immunosuppressive protocols have used a combination of drugs that significantly decreased the rate of acute organ rejection. Despite advances in surgical and medical care of recipients of solid-organ transplants, long-term graft survival and patient survival have not improved during the past 2 decades. Current immunosuppression protocols include a combination of calcineurin inhibitors, such as tacrolimus, and antiproliferative agents (most commonly mycophenolate mofetil), with or without different dosing regimens of corticosteroids. Mammalian target of rapamycin inhibitors were introduced to be used in combination with cyclosporine-based therapy, but they did not gain much acceptance because of their adverse event profile. Belatacept, a costimulatory inhibitor, is currently being studied in different regimens in an effort to replace the use of calcineurin inhibitors to induce tolerance and to improve long-term outcomes. Induction therapy is now being used in more than 90% of kidney transplants and more than 50% cases of other solid-organ transplantation such as lung, heart, and intestinal transplants. As a result of these combination immunosuppressive (IS) therapy protocols, not only the incidence but also the intensity of episodes of acute rejection have decreased markedly, and at present 1-year graft and patient survival is almost 98% for kidney transplant recipients and approximately greater than 80% for heart and lung transplants. Evolving concepts include the use of donor-derived bone marrow mesenchymal cells to induce tolerance, to minimize the use of maintenance IS agents, and to prevent the development of adverse events associated with long-term use of maintenance IS therapy.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(2). DOI:10.1615/CritRevEukaryotGeneExpr.2015011421
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    ABSTRACT: Mesenchymal stem cells (MSCs) have 2 specific characteristics: self-renewal and multi- or pluripotency. Extensive studies have demonstrated the regenerative capability of MSCs both in vitro and in vivo. Gingiva-derived MSCs (GMSCs) represent a unique population of MSCs that can be easily isolated and obtained. GMSCs, which maintain a normal karyotype and telomerase activity in long-term cultures, display a stable phenotype and rapidly proliferate in vitro. In addition, GMSCs can be induced to differentiate into osteogenic, chondrogenic, and adipogenic lineages. Therefore, GMSCs are a promising alternative cell source for tissue regeneration in dentistry. In this article we review studies of the characterization, differentiation capacities, and regenerative role of GMSCs derived from the gingiva of humans and other species, focusing on the mechanisms of differentiation and tissue regeneration of human GMSCs. We anticipate that GMSC-based therapies will significantly contribute to regenerative medicine for the treatment of human dental diseases and improve human health.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(2). DOI:10.1615/CritRevEukaryotGeneExpr.2015012539
  • Critical Reviews in Eukaryotic Gene Expression 01/2015; DOI:10.1615/CritRevEukaryotGeneExpr.2015013838
  • Critical Reviews in Eukaryotic Gene Expression 01/2015; DOI:10.1615/CritRevEukaryotGeneExpr.2015013893
  • Critical Reviews in Eukaryotic Gene Expression 01/2015; DOI:10.1615/CritRevEukaryotGeneExpr.2015013843
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    ABSTRACT: Cells are exposed to diverse stresses; poly(ADP-ribose) polymerase-1 (PARP-1), which processes diverse signals and directs cells to specific fates (survival or death), is a key player in responses to cellular stress. PARP-1 usually uses NAD+ as a donor of ADP-ribose units to regulate the synthesis of poly(ADP-ribose). Over 100 novel substrates of PARP-1 have been identified, most of which are involved in cellular processes such as ribosome biogenesis and transcription regulation. In addition, PARP-1 functions in inflammation by modulating inflammatory-relevant gene expression. PARP-1 also is involved in the tissue damage caused by ischemia/reperfusion conditions. Common inflammatory mediators (inducible nitric oxide synthase, interleukin [IL]-1β, and tumor necrosis factor-α) are regulated by PARP-1, which helps amplify nuclear factor-κB-mediated inflammation. PARP-1 plays a role in adaptive immunity by modulating the ability of dendritic cells to stimulate T cells. The expression of several genes (such as IL-2 and IL-10) and T-cell proliferation also are controlled by the activation of PARP-1. Inhibition of PARP-1 enzymatic activity attenuates the secretion of proinflammatory cytokines and therefore alleviates autoimmune diseases. PARP inhibitors may represent a new avenue for disease treatment.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(2):175-90.
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    ABSTRACT: Natriuretic peptide receptor A (NPR-A) is the receptor for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). NPR-A plays critical physiological and pathophysiological roles in several target cell and tissue system processes, such as cell growth, apoptosis, proliferation, and inflammation. Accumulating data demonstrate that NPR-A is involved in immune and inflammatory reactions and is a potential target in inflammation treatment. It is expressed in various cancer cells and is important for tumor growth. A recent study indicated that NPR-A signaling can regulate stem cell recruitment and angiogenesis. This signaling can serve as a model for studying the linkage between inflammation and tumorigenesis. In this review we highlight the mechanisms by which NPR-A affects signaling pathways involved in inflammation and cancer, and we discuss its potential as a novel target in inflammation, cancer, and cancer-related inflammation.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(1). DOI:10.1615/CritRevEukaryotGeneExpr.2015012447
  • Critical Reviews in Eukaryotic Gene Expression 01/2015; DOI:10.1615/CritRevEukaryotGeneExpr.2015013057
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    ABSTRACT: Intracellular bacterial pathogens drive the formation of host membrane-derived pseudo-organelles that facilitate their replication, survival, or dormancy. The formation and maintenance of these bacteria-containing vacuoles (BCVs) are dependent on the bacteria's ability to usurp the host's intracellular membrane system, in particular dynamic compartments involved in exo-/endocytic membrane traffic and autophagy. Bacteria are typically internalized by phagocytosis, and the compartment matures through endosomal fusion. The bacteria-containing phagosome/endosome often becomes the base for BCV formation. Diverse strategies used by different bacterial pathogens prevent the BCV from being destroyed via the endolysosomal pathway. Furthermore, bacterial survival or proliferation in BCVs could be augmented by host membrane transport processes subverted by secreted bacterial factors, which facilitate the acquisition of membrane sources and nutrients. BCVs may be targeted for destruction by autophagy, and various facultative and obligate intracellular bacteria have evolved ways to evade or even exploit autophagy. Here we review examples of bacterial subversion of host cellular membrane transport and autophagy machinery for a productive invasion.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(2). DOI:10.1615/CritRevEukaryotGeneExpr.2015013572
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    ABSTRACT: Epidemiologic studies have suggested that South Korea is a country with low risk rates of osteoporosis and osteoporotic fractures. Recently, the Korean Nationwide-Databased Osteoporosis Study (KNOS) performed an overall analysis of osteoporosis using data from the Health Insurance Review and Assessments (HIRA) database. The Korean National Health Insurance Program covers almost 100% of the Korean population, and HIRA reviews all information on medication, operation, and discharge diagnoses according to ICD-10 codes. Therefore, all information about osteoporosis and osteoporotic fractures was obtained from this centralized database. This article reviews the KNOS's efforts to characterize the management of osteoporosis in South Korea.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(1). DOI:10.1615/CritRevEukaryotGeneExpr.2015012425
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    ABSTRACT: Autophagy, a highly conserved self-degradation process that occurs under both physiological and pathological conditions, provides the raw material and energy for cell regeneration under normal circumstances. Dysregulated autophagy under diseased conditions may cause protein accumulation, organelle dysfunction, and even cell death. Recent studies have shown that autophagy regulates the structural integrity and physiological functions of retinal photoreceptor cells and contributes to the pathogenesis of retinopathies such as retinal detachment, age-related macular degeneration, retinitis pigmentosa, and Leber's congenital amaurosis. In this review, we discuss the role of autophagy in photoreceptor cell survival and death in retinal physiology and diseases, and suggest the possibility that autophagy-targeting therapy may be a new strategy for retinal diseases marked by photoreceptor cell death.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(1). DOI:10.1615/CritRevEukaryotGeneExpr.2015012376
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    ABSTRACT: Semaphorin 3A (Sema3A), characterized by a conserved N-terminal "Sema" domain, was originally described as an axon guidance molecule. Recent research indicates that it performs a critical function in the skeletal system. This review highlights recent advances in understanding of the role of Sema3A in the skeletal system as a regulator of bone metabolism and as a potential drug target for bone disease therapy. We summarize Sema3A functions in osteoblastogenesis and osteoclastogenesis, as well as in innervation, and we discuss its multifunctional role in various bone diseases such as osteoporosis and low back pain. Despite limited research in this field, our aim is to promote further understanding of the function of Sema3A in the skeletal system
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(1). DOI:10.1615/CritRevEukaryotGeneExpr.2015012469
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    ABSTRACT: Bone is an important porous tissue that supports the body, maintains calcium and phosphate homeostasis, protects vital organs, and houses bone marrow. The interaction between hydrostatic pressure and fluid phase, solid phase, cells, and vascular in bone makes bone inevitably bear baseline levels of fluid flow. Fluid flow plays an important role in regulating the proliferation, differentiation, distribution, and apoptosis of osteoblasts in bone. The effect of fluid flow on osteoblasts is dependent on time, velocity, and type. Some response of osteoblasts to fluid flow is closely related to the soluble factors secreted by the osteoblasts themselves or other types of bone cells. When the response is disordered, related bone diseases such as osteoporosis, osteoarthritis, and abnormal osteogenesis probably happen. In this article we review the current progress in the study of the response of osteoblasts to the direct and indirect stimulus of fluid flow and their roles in osteogenesis and related bone diseases.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(2). DOI:10.1615/CritRevEukaryotGeneExpr.2015013564
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    ABSTRACT: Adipose tissue has emerged as an attractive cell source in tissue engineering and regenerative medicine because it can be easily collected and enriched with stem/progenitor cell populations. The stromal vascular fraction (SVF) derived from adipose tissue contains heterogeneous cell populations such as mesenchymal progenitor/stem cells, preadipocytes, endothelial cells, pericytes, T cells, and M2 macrophages. SVF-derived mesenchymal progenitor/stem cells can be easily expanded in vitro and have the potential to create diverse lineages of cells. Although there have been issues related to their isolation and purification, SVF cells demonstrate regenerative potential in damaged tissues or organs through paracrine and differentiation mechanisms. Furthermore, SVF cells augment immunological tolerance by promoting inhibitory macrophages and T regulatory cells and by decreasing ongoing inflammation. Numerous implantations of freshly isolated, autologous adipose tissue-derived SVF cells in cosmetic surgeries and in a wide variety of other specialties support the safety of SVF cells and have accelerated their clinical application. Despite these attractive advantages of SVF cells in clinical interventions, to our knowledge the recent status of clinical studies of various diseases has not been fully investigated. Therefore this article describes recent advances in the clinical use of SVF cells, as well as the associated challenges and future directions for this field of research. We also speculate that verification of the efficacy and safety of SVF cells requires more basic experimental research, using a standard isolation protocol, and larger randomized clinical trials of the utility of SVF cells in various diseases.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(2):145-52.
  • Critical Reviews in Eukaryotic Gene Expression 01/2015; DOI:10.1615/CritRevEukaryotGeneExpr.2015013929
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    ABSTRACT: Posttranscriptional gene regulation is a rapid and effective way to mediate the expression of inflammatory genes. CCCH-type zinc finger proteins are nucleotide-binding molecules involved in RNA metabolism pathways such as RNA splicing, polyadenylation, and messenger RNA (mRNA) decay. Among these proteins, tristetraproline, Roquins, and Regnase-1/monocyte chemotactic protein-1-induced protein-1 have been recently reported to be responsible for mRNA instability. They bind to mRNAs harboring unique motifs and induce mRNA decay. In this review we summarize current progress regarding the specific characteristics of sequences and structures in the 3' untranslated regions of mRNAs that are recognized by tristetraproline, Roquins, and Regnase-1. The target mRNAs to be destabilized by those CCCH-type zinc finger proteins also are included. Notably, most target mRNAs encode cytokines and other inflammatory mediators, suggesting the immune regulation role of CCCH zinc finger proteins. Mice carrying a genetic null allele or modification of these genes display severe symptoms of autoimmune diseases. Taken together, data show that CCCH-type zinc finger proteins play a crucial role in regulating immune response by targeting multiple mRNAs, and including decay. Further understanding the functions of these proteins may provide new therapeutic targets for immune-related disorders in the future.
    Critical Reviews in Eukaryotic Gene Expression 01/2015; 25(1). DOI:10.1615/CritRevEukaryotGeneExpr.2015013022