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: 1.57

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 1.571
2013 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

Additional details

5-year impact 3.06
Cited half-life 6.30
Immediacy index 0.24
Eigenfactor 0.00
Article influence 0.98
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
    • Publisher's version/PDF cannot be used
    • Publisher last reviewed on 25/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Nemo-like kinase (NLK) is an evolutionarily conserved mitogen-activated protein (MAP) kinase-related kinase that is highly expressed in neural tissues and minimally detected in others. Accumulating evidence demonstrates that NLK exerts a pivotal role in cell proliferation, migration, invasion, and apoptosis via regulation of a variety of transcriptional molecules. The results of recent studies have shown that aberrant expression of NLK is significantly associated with the initiation and progression of various types of human cancers, as well as clinicopathologic features and survival rate. NLK is gradually considered as a potential tumor suppressor or an oncogene depending on the tumor system, and silencing or upregulating of NLK may provide an effective therapeutic approach against tumors. In this review, we will make a summary on the comprehensive roles of NLK in the regulation of various cancers.
    Critical Reviews in Eukaryotic Gene Expression 10/2015; DOI:10.1615/CritRevEukaryotGeneExpr.2015013966
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    ABSTRACT: A cancer positive-feedback loops conversion is the phenomenon and principal mechanism for AKT locus chemotherapy. Such chemotherapy is the approach to target cancer robustness and complexity through the AKT signaling locus. The hypoxic cancer microenvironment generates a powerful signaling interactome with positive-feedback loops that generates cancer robustness through the AKT locus. This complexity and robustness can be successfully halted in leukemia, lymphoma, myeloma, plasmocytoma, sarcoma, and carcinoma by converting cancer positive-feedback loops into negative-feedback loops, achieved through the AKT dephosphorylation by redox balancing change. The hyperphosphorylated AKT locus is down-regulated completely to AKT dephosphorylation by redox balancing change, causing conversion of positive-feedback loops and the disappearance of malignant robustness as a direct effect of AKT locus chemotherapy.
    Critical Reviews in Eukaryotic Gene Expression 09/2015; 25(3). DOI:10.1615/CritRevEukaryotGeneExpr.2015013838
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    ABSTRACT: Various types of cancer continue to be subjects of intense research because of the impact of these diseases and their socioeconomic implications. Also, the complexity involved in the pathogenesis, nature of the triggers, and the progression of cancers is intriguing. An important aspect of cancers is the genetics involved, and studies involving cancer genes contributed immensely in not only understanding cancers better, but also for obtaining useful markers and therapy targets. We review the salient features, functions, and changes in gene expression for 103 carcinoma genes, 20 sarcoma genes, and 36 lymphoma genes. Apart from the three major levels of cancer type, we discuss the implications of altered gene expression at the tissue level as well. The possible uses of these gene functions and expression changes for diagnostic, prognostic, and therapeutic applications are presented. Also, the 159 genes are assessed for their involvement in more than a single cancer and tissue type. Only the p53 gene is commonly implicated in carcinomas, sarcoma and lymphomas. The CHEK2 and ERBB2 (HER2) genes are commonly found to be associated with carcinomas and sarcomas, whereas the MDM2, MSH2, and MSH6 genes are commonly implicated among carcinomas and lymphomas.
    Critical Reviews in Eukaryotic Gene Expression 09/2015; 25(3):209–238. DOI:10.1615/CritRevEukaryotGeneExpr.2015013893
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    ABSTRACT: Mushroom extracts have been extensively studied for their medicinal effects. They can stimulate immune responses and thus have been explored in cancer treatment. Recently, it has also been shown that some mushroom extracts can produce direct cytotoxic effect on cancer cells. In this review, we summarize the cytotoxic effect of mushroom extracts in cancer treatment revealed by both in vitro and in vivo studies. We also summarize the current understanding of the mechanisms associated with such an effect with an emphasis on the mitochondrial apoptotic pathway. The recent finding that mushroom extracts have direct cytotoxic effects supplements their known immune stimulating effects. Thus, novel anticancer agents based on new findings from mushroom extracts may soon be added to the present pool of anticancer drugs. Specifically, we propose that nanodelivery of the bioactive compounds of mushroom extracts to mitochondria will further increase their potential treatment efficacy.
    Critical Reviews in Eukaryotic Gene Expression 09/2015; 25(3). DOI:10.1615/CritRevEukaryotGeneExpr.2015014019
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    ABSTRACT: Long non-coding RNA (lncRNA) is a type of DNA transcript that is longer than 200 nucleotides (nt). They do not encode proteins, but they control gene expression on various levels. Long non-coding RNA metastasisassociated urothelial carcinoma associated 1 (UCA1) was confirmed to play an important role in the occurrence and development of many tumor and non-tumor diseases. UCA1 mainly interacts with proteins in the nucleus, regulating gene expression in transcription and post-transcription. UCA1 is highly expressed in tumor tissue, and therefore can be related to clinical parameters. It may regulate tumor cell proliferation, invasion, apoptosis, and migration, so UCA1 can be applied in clinical prognosis and targeted therapy. This review mainly elaborates the roles of UCA1 in tumor diseases of the respiratory, digestive, reproductive, and urinary systems; and in non-tumor diseases.
    Critical Reviews in Eukaryotic Gene Expression 09/2015; 25(3). DOI:10.1615/CritRevEukaryotGeneExpr.2015013770
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    ABSTRACT: Protein N-myristoylation is a ubiquitous cotranslational and posttranslational modification catalyzed by myristoyl CoA:protein N-myristoyltransferase (NMT), which attaches myristate, a rare 14-carbon saturated fatty acid, to an N-terminal glycine of some eukaryotic and virus proteins. This protein modification triggers dynamic protein– protein and protein–membrane interactions implicated in diverse physiological processes. This review summarizes the NMT catalytic mechanism and demyristoylation. Of special interest are the primary roles of N-myristoylated protein in signaling, protein targeting, tumorigenesis, apoptosis, virus assembly, and morphology change, as well as the regulation of N-myristoylation and NMT inhibitors.
    Critical Reviews in Eukaryotic Gene Expression 09/2015; 25(3). DOI:10.1615/CritRevEukaryotGeneExpr.2015013978
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    ABSTRACT: Chronic inflammation, such as that seen in patients with inflammatory bowel disease (IBD), greatly increases the risk of developing colon cancer. Growing evidence supports a role for T cell–mediated immune response and release of various cytokines in the pathogenesis of colitis-associated cancer (CAC). In fact, CD4+ effector T cells promote chronic inflammation associated with IBD through release of proinflammatory cytokines, which leads to initiation and progression of colon cancer. Furthermore, CD8+ T cells reduce tumor growth through cancer immunosurveillance, which can also contribute to intestinal inflammation and thereby might promote tumor growth. In contrast, regulatory T cells (Tregs) release the immunosuppressive cytokines IL-10, TGF-b, and thus have protective effects in CAC. In addition, dendritic cells (DCs) are important components of antitumor immunity. Recently, a novel mouse model that was associated with repeated inflammation was established for investigating the immunopathogenesis of CAC. This review discusses the role of T cell–mediated immune response, and DCs and involved cytokines in the immunopathogenesis of CAC in an animal model, which may also provide future therapeutic targets in CAC.
    Critical Reviews in Eukaryotic Gene Expression 09/2015; 25(3). DOI:10.1615/CritRevEukaryotGeneExpr.2015013885
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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 06/2015; 25(2). DOI:10.1615/CritRevEukaryotGeneExpr.2015012539
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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 06/2015; 25(2). DOI:10.1615/CritRevEukaryotGeneExpr.2015011421
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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 06/2015; 25(2):175-90. DOI:10.1615/CritRevEukaryotGeneExpr.2015013626
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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 06/2015; 25(2). DOI:10.1615/CritRevEukaryotGeneExpr.2015013572
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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 06/2015; 25(2):145-52.
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    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 05/2015; 25(1). DOI:10.1615/CritRevEukaryotGeneExpr.2015012369
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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 05/2015; 25(1). DOI:10.1615/CritRevEukaryotGeneExpr.2015012425