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Publisher: Smart Science and Technology LLC   (Total: 21 journals)   [Sort by number of followers]

Showing 1 - 21 of 21 Journals sorted alphabetically
Abdomen     Open Access  
Cancer Cell & Microenvironment     Open Access   (Followers: 9)
Cardiovascular Regenerative Medicine     Open Access  
Evidence-based Medicine & Public Health     Open Access   (Followers: 7)
Immunoendocrinology     Open Access   (Followers: 1)
Inflammation and Cell Signaling     Open Access   (Followers: 3)
Itch & Pain     Open Access   (Followers: 2)
J. of Advanced Nutrition and Human Metabolism     Open Access   (Followers: 14)
Macrophage     Open Access  
Molecular & Cellular Epilepsy     Open Access   (Followers: 2)
Musculoskeletal Regeneration     Open Access   (Followers: 2)
Neurotransmitter     Open Access  
Precision Medicine     Open Access   (Followers: 2)
Receptors & Clinical Investigation     Open Access   (Followers: 1)
RNA & Disease     Open Access   (Followers: 1)
Science Proceedings     Open Access   (Followers: 1)
Stem Cell and Translational Investigation     Open Access   (Followers: 2)
Stem Cell Epigenetics     Open Access   (Followers: 3)
Telomere and Telomerase     Open Access  
Therapeutic Targets for Neurological Diseases     Open Access   (Followers: 1)
Uterus & Ovary     Open Access  
Journal Cover
Stem Cell Epigenetics
Number of Followers: 3  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2378-3095
Published by Smart Science and Technology LLC Homepage  [21 journals]
  • An effective mass-spectrometry- based strategy for characterizing histone
           H3K9 modifications

    • Authors: Ho-Geun Kwak, Naoshi Dohmae
      Abstract: Abstract Mass spectrometry (MS)-based analytical approaches to examine histone post-translational modifications (PTMs) are useful tools to understand epigenetic function. Histone H3K9 methylation plays an important role in chromatin remodeling, which is important in stem cell self-renewal and differentiation. With a simple, rapid, and accurate top-down strategy using matrix assisted laser desorption/ionization (MALDI)-in source decay (ISD), we have recently identified K9 PTMs on H3 variants (H3.1, H3.2, H3.3, and H3t) in the mouse testis. Mono-, di-, and tri-methylated K9 sites were identified on H3 variants separated using liquid chromatography and an ion-pairing reagent. These modifications were also observed in the testis-specific histone H3 using MALDI-ISD. Our findings demonstrate a novel top-down approach for characterizing PTMs on histone tails that will have applications in future research. Keywords: MALDI-ISD, Testis-specific H3 histone, K9 modifications
      PubDate: 2017-02-06
      DOI: 10.14800/sce.1501
      Issue No: Vol. 4 (2017)
       
  • Antitumour effects of artichoke polyphenols: cell death and ROS-mediated
           epigenetic growth arrest

    • Authors: Anna Maria Mileo, Donato Di Venere, Stefania Miccadei
      Abstract: Abstract  Many epidemiological studies suggest that diet particulary rich in fruit and vegetables have cancer preventive properties. The beneficial effects of these diets are attributable, at least in part,  to polyphenols that have emerged as very promising anticancer bioactive compounds. We report that polyphenolic extracts from the edible part of artichoke show a potential chemopreventive and anticancer properties on several cancer cell lines. High dose of extracts of artichoke (AEs) reduced cell viability and inhibited cell growth in a dose dependent-manner. In particular AEs triggered apoptosis and modulate other tumour related features such as migration and invasion in highly metastatic breast cancer cells. In addition, we provide evidences that low dose of AEs-treatment inhibits breast cancer cell growth via the induction of premature senescence through epigenetic and ROS-mediated mechanisms. These findings demonstrated that high dose-AEs activate apoptotic machinery whereas low level treatment induce senescence in cancer cells. Since apoptosis and cellular pro-senescence are considered relevant anticancer therapeutic mechanisms, artichoke polyphenols extracts from the edible part, could be a promising dietary tool either in cancer chemoprevention or/and in cancer treatment as a non-conventional, adjuvant therapy.  
      PubDate: 2016-04-04
      DOI: 10.14800/sce.1242
      Issue No: Vol. 3 (2016)
       
  • Mitochondrial DNA alteration and pathological progression in colorectal
           cancer

    • Authors: Jinhang Gao, Shilei Wen, Hongying Zhou, Shi Feng
      Abstract: Mitochondrion, the major organelle involved in cell energy metabolism, plays important roles in many human diseases. Nowadays, its dysfunction during initation and progression of cancers is calling more and more attention. Since Otto Warburg brought out his hypothesis, mitochondrial DNA (mtDNA) may affect on cancer development by regulating oxidative phosphorylation, many important findings have been discovered. It is widely recognized that research the potential correlations between mitochondrion and mtDNA in cancers are of great importance. And the trends of change of mtDNA content are different in different cancers. Thus leaves us numerous works to do. Although some cancers have already been reported their relation with mtDNA alteration, different experimental methods or evidence may lead to different conclusions. This article presents a brief in summarizing the mitochondrion dysfunction in human disease and the alteration of mtDNA in cancers. Moreover, the recent highlighting achievements on colorectal cancer and mtDNA are also summarized to provide a discussion on possible pathological mechanism and clinical usage.
      PubDate: 2016-01-18
      DOI: 10.14800/sce.1144
      Issue No: Vol. 3 (2016)
       
  • Male fertility: Genome integrity and sperm DNA methylation

    • Authors: Debbie Montjean, Célia Ravel
      Abstract: Male infertility is a complex multifactorial pathology that is correlated in some extent with semen parameters including sperm counts, motility, morphology, viability and nucleus integrity. The large debate surrounding global decline of semen parameters motivated numerous studies dealing with this important issue. The present article reviews different factors shown to impact on male fertility by affecting semen parameters, namely, epigenetics and sperm genome integrity.
      PubDate: 2015-12-21
      DOI: 10.14800/sce.1106
      Issue No: Vol. 3 (2015)
       
  • HDAC9/miR-376a feed-forward loop drive tumorigenesis in hepatocellular
           carcinoma

    • Authors: Yongxia Zheng, Huan Chen
      Abstract: microRNA and epigenetic mechanism usually influence each other and evoke tumorigenesis in HCC. Aberrations of miR-376a have been observed in HCC, but the factors that contribute to the aberrations have not been fully elucidated. Histone acetylation enzyme, as an important epigenetic mechanism, is invoved in the deregulation of microRNAs. HDAC9 is a potential target gene of miR-376a by bioinformatics analysis, we determined it. Interestingly, we found that HDAC9-mediated epigenetic modification may contribute to the down-regulation of miR-376 cluster in HCC. In turn, decreased miR-376a partially resulted in up-regulation of HDAC9 in HCC. In sum, our results highlight the importance of feedback regulation in building epigenetic memory.
      PubDate: 2015-03-29
      DOI: 10.14800/sce.726
      Issue No: Vol. 3 (2015)
       
  • Epigenetic modification in congenital heart diseases by using stem cell
           technologies

    • Authors: Hidemasa Oh
      Abstract: Congenital heart diseases are the most common birth defects, occurring in more than 1% of newborns. The gene regulatory network of cardiac development has been revealed and some cases of congenital heart diseases have been shown to be associated with cardiac-specific gene mutations or related chromosomal abnormalities; however, almost all cases of congenital heart diseases are sporadic and the pathogenesis of heart malformations still remains unknown. Recently, studies of epigenetic regulation have been making progress in the field of cardiac development and the accumulated knowledge helps us understand more about cardiogenesis and congenital heart diseases. Interestingly, pluripotent stem cells such as embryonic stem (ES) cells and induced pluripotent stem (iPS) cells have attracted attention as tools to dissect epigenetic regulation during differentiation. Reprogramming and differentiation of ES cells and iPS cells can be induced by changes of gene expression patterns and epigenetic regulation, not by changing DNA sequences. We can also modify histone patterns and chromatin structures using chemical reagents. Hence, pluripotent stem cells enable us to dissect and modify epigenetic regulation during cardiogenesis in vitro. Moreover, in terms of iPS cells, they have become disease models because they can be generated from the somatic cells of patients. In this review, we summarize the recent findings of epigenetic regulation in cardiac development and congenital heart diseases. We also review the epigenetic modification during the reprogramming and cardiac differentiation of ES cells and iPS cells, and introduce our study showing that the disease-specific iPS cells of hypoplastic left heart syndrome, one of the severest congenital heart diseases with single ventricular circulation, exhibit unique epigenetic regulation during differentiation. Furthermore, we briefly focus on modifications of epigenetic regulation in cardiac development using chemical reagents, which suggest the possibility of treating congenital heart diseases using drugs. Lastly, we discuss the epigenetic memory of iPS cells, a specific feature that often complicates or prevents study of the differentiation of iPS cells.
      PubDate: 2015-02-15
      DOI: 10.14800/sce.550
      Issue No: Vol. 3 (2015)
       
  • Bacterial Short Chain Fatty Acids Push All The Buttons Needed To
           Reactivate Latent Viruses

    • Authors: Fengchun Ye, Jonathan Karn
      Abstract: The genomes of herpesviruses and HIV become silent during latency through multiple chromatin silencing mechanisms including: histone deacetylation, repressive histone methylation, and DNA methylation.  Reactivation of the latent virus requires removal of the chromatin silencing marks and their replacement by activating modifications such as histone acetylation and activating histone methylation. In a complementary mechanism, RNA Polymerase II (RNAP II) elongation is regulated by the positive transcription elongation factor b (P-TEFb)-dependent phosphorylation of Ser2 residues on its C-terminal domain. In resting T-cells latently infected by HIV P-TEFb levels are extremely low. We found that a group of short chain fatty acids (SCFAs) produced by oral bacteria not only promote histone acetylation but also changes the histone methylation dynamics by decreasing repressive histone methylation while increasing activating histone methylation.  SCFAs also block DNA methylation and activate P-TEFb to enable elongation of stalled RNA polymerase II.  Thus these molecules do not simply act as histone deacetylase (HDAC) inhibitors as previously claimed.  Instead, they impact multiple complementary epigenetic regulatory mechanisms to promote highly efficient reactivation of latent viruses.
      PubDate: 2015-01-28
      DOI: 10.14800/sce.532
      Issue No: Vol. 3 (2015)
       
  • Targeting AML stem/progenitor cells by combinational therapy with SMAC
           mimetics and demethylating agents

    • Authors: Michael Andreeff
      Abstract: Chemotherapy for acute myeloid leukemia (AML) principally induces intrinsic apoptosis in circulating leukemic blasts. Unfortunately, standard therapy is relatively ineffective in eliminating AML stem/progenitor cells that drive leukemogenesis. The inhibitors of apoptosis (IAP) protein family are critical regulators of cell survival. IAP proteins, in particular cIAP1 and cIAP2, have drawn great attention in recent years as targets for cancer therapy due to the development of SMAC mimetics. We discovered that the expressions of cIAP1, which primarily inhibits the extrinsic apoptosis pathway and a main target of SMAC mimetics, and caspase-8, the key caspase of the extrinsic apoptosis were significantly higher in AML stem/progenitor cells than in bulk AML cells. Conversely, the expression of SMAC, an endogenous antagonist of IAP proteins, was significantly lower by comparison. We investigated the therapeutic potential of targeting IAPs by SMAC mimetics in AML and reported that the novel SMAC mimetic birinapant effectively induced apoptosis in AML cells, including AML stem/progenitor cells. This effect was present even in leukemic cells co-cultured with bone marrow derived-mesenchymal stromal cells under hypoxic conditions representative of the bone marrow microenvironment. Furthermore, this anti-leukemia activity was enhanced in vitro and in vivo by combination with demethylating agents, which apparently modulated NFkB signaling and many key members of the extrinsic apoptosis pathway. The apoptosis repressor with caspase recruitment domain (ARC) protein is known to suppress the extrinsic apoptosis. We have demonstrated that ARC is an effective negative prognostic factor for AML, is regulated by cIAP1/NIK signaling in AML cells, and can be inhibited by demethylating agents. Our findings suggest that the activation of the extrinsic pathway has the potential to eradicate AML stem/progenitor cells and that mechanistic combinations of SMAC mimetics with agents that modulate the extrinsic apoptosis pathway may benefit patients with AML. In fact, our preliminary results served as the catalyst for recently-initiated phase I/II trials of birinapant in combination with 5-azacytidine in pre-leukemia myelodysplastic syndrome and AML patients.
      PubDate: 2015-01-28
      DOI: 10.14800/sce.525
      Issue No: Vol. 3 (2015)
       
  • Setdb1 is implicated in the methylation of pericentric satellite DNA

    • Authors: Yong-Kook Kang
      First page: 10
      Abstract: Setdb1/Eset, a histone H3-lysine 9 (H3K9)-specific methyltransferase, interacts with various transcription factors to modify chromatin at target genomic regions. In this study, we provide evidence supporting that Setdb1 also regulates genomic DNA methylation. Whereas 5-methylcytosine (5-mC) signal majorly localizes at pericentric heterochromatin regions in wild type cells, knocking down Setdb1 resulted in diffuse localization of 5-mC signal. Setdb1 knockdown also reduced the expression and subcellular localization of the DNA methyltransferases Dnmt1 and Dnmt3a. Bisulfite mutagenesis studies revealed that Setdb1 knockdown reduced the methylation of satellite DNA sequences (heterochromatin) but not of intracistronic A particle (IAP) sequences (euchromatin). Our results suggest that Setdb1 directly or indirectly regulates the expression of DNA methyltransferases and thus affects DNA methylation and the structural organization of heterochromatin.
      PubDate: 2015-08-13
      DOI: 10.14800/sce.938
      Issue No: Vol. 2, No. 2 (2015)
       
  • The role and epigenetic regulation of the CDX gene family in human cancer

    • Authors: Mingzhou Guo, Yan Dong
      First page: 10
      Abstract: The caudal (Cdx) family of DNA binding proteins was originally identified in Drosophila; however, homologues with conserved molecular structure and function have been described in several organisms including humans. The three members of the Cdx family in mice and humans, Cdx1, Cdx2, and Cdx4, have been intensively studied for their involvement in axial elongation and early antero-posterior patterning. Cdx1 and Cdx2 regulate cell growth and differentiation, and they are involved in embryonic development of the intestinal tract, intestinal inflammation and tumorigenesis. In colon cancer, CDX1 and CDX2 suppress colon cell proliferation, migration and invasion by inhibiting β-catenin/TCF transcriptional activity. The expression of CDX1 and CDX2 exists in intestinal metaplasia but not in normal gastric and esophageal mucosa. CDX genes are overexpressed in leukemias. The changes in expression levels of Cdx genes correlate with oncogenic transformation. CDX2 serves as a Wnt signaling inhibitor and is frequently methylated in lung cancer. CDX2 methylation is also a feature of human esophageal squamous cancer, and it may serve as a cancer detection marker.
      PubDate: 2015-07-06
      DOI: 10.14800/sce.882
      Issue No: Vol. 2, No. 2 (2015)
       
  • Hypothetical Epigenetic Fingerprint in Nutritional-Neural-microbiota
           Connection

    • Authors: Olaposi Idowu Omotuyi
      First page: 10
      PubDate: 2015-06-24
      DOI: 10.14800/sce.863
      Issue No: Vol. 2, No. 2 (2015)
       
  • Expanding the genetic code to study metalloproteins and protein
           posttranslational modifications

    • Authors: Qing Zhou, Lu Hao
      First page: 10
      Abstract: In order to expand the genetic code to study metalloproteins and protein posttranslational modifications, we constructed several tyrosine and pyrrolysyl-tRNA synthetase libraries based on tyrosine and pyrrolysyl-tRNA synthetase/tRNA pairs to expand the genetic code, to screen unnatural amino acids with similar chemical structure to tyrosine or lysine. We had incorporated several unnatural amino acids into proteins, including metal-chelating, proton and electron transfer mediators, bioorthogonal reaction groups containing amino acids, and played a series of bio-orthogonal reactions in vivo and in vitro, such as copper click of azide and alkyne, copper free click of azide and cycloalkyne, photoclick of alkene and tetrazole, which laid the foundation for proteins specifically labeling, protein-protein interaction probing, and biological processes photo-regulation. Besides that, we applied this method to incorporate redox unnatural amino acids to improve the property of fluorescent proteins. We explored the activities of proteins and downstream signaling pathways by using sulfur or fluorine mimetics of acetylated lysine as probes of protein posttranslational modifications. We also directed Nε-Formyl-L-lysine into histones to study the impact of Nε-formylation of lysine naturally caused by oxidative damage in cells on histones.
      PubDate: 2015-06-15
      DOI: 10.14800/sce.854
      Issue No: Vol. 2, No. 2 (2015)
       
  • Mathematical modeling of cell-fate specification: From simple to complex
           epigenetics

    • Authors: Jomar Fajardo Rabajante, Ariel Lagdameo Babierra, Jerrold Maranan Tubay, Editha Carreon Jose
      First page: 10
      Abstract: Modern biology will never be the same without mathematical and computational tools. Using mind map with “epigenetics” as the root, we discuss the current advancement in the field of biomathematics for modeling cell-fate specification. In the discussions, we also present possible directions for future research.
      PubDate: 2015-04-07
      DOI: 10.14800/sce.752
      Issue No: Vol. 2, No. 2 (2015)
       
  • Pharmacoepigenetics explores the epigenetic contribution to anti-cancer
           agent-induced cytotoxicities

    • Authors: Xu Zhang, Wei Zhang
      Abstract: Elucidating genetic and epigenetic contributions to drug response variation is critical for the realization of personalized medicine, which may particularly benefit cancer patients, for whom anti-cancer agent-induced cytotoxicities are often major adverse reactions. Previous pharmacogenomic discoveries have utilized the HapMap lymphoblastoid cell line (LCL) model, on which the research community has accumulated extensive genotypic data and gene expression profiles. Given the complex nature of gene expression regulation, expanding the cell-based model to include epigenetic systems such as cytosine modifications has begun to allow novel pharmacoepigenetic studies that may enhance our understanding of drug response variation. Using a collection of the HapMap LCL samples, our team has profiled the genome-wide cytosine modification levels and explored the contribution of CpG modifications to anti-cancer agent-induced cytotoxicities. Specifically, in our recent pharmacogenomic study on clofarabine, we demonstrated that by integrating cytosine modifications, genetic variants, and gene expression phenotypes, we were able to significantly improve our ability to explain the phenotypic variance among individuals. Finally, advances in experimental techniques that can distinguish 5’-methylcytosine (5mC) and 5’-hydroxymethylcytosine (5hmC), the latter of which is a recently rediscovered nucleotide base in the human genome with potential unique biological functions, as well as stem cell technologies that can differentiate target tissues from induced pluripotent stem cells (iPSCs), will move forward the current pharmacoepigenetic and pharmacogenomic research to the next stage with higher molecular resolution and better clinical relevance. 
      PubDate: 2014-10-06
      DOI: 10.14800/sce.359
      Issue No: Vol. 3 (2014)
       
 
 
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