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  • 1
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    Promoter occupancy of the basal class I transcription factor A differs strongly between active and silent VSG expression sites in Trypanosoma brucei (2014)
    Oxford University Press
    Details
    Publication Date: 2014-03-13
    Description: Monoallelic expression within a gene family is found in pathogens exhibiting antigenic variation and in mammalian olfactory neurons. Trypanosoma brucei , a lethal parasite living in the human bloodstream, expresses variant surface glycoprotein (VSG) from 1 of 15 bloodstream expression sites (BESs) by virtue of a multifunctional RNA polymerase I. The active BES is transcribed in an extranucleolar compartment termed the expression site body (ESB), whereas silent BESs, located elsewhere within the nucleus, are repressed epigenetically. The regulatory mechanisms, however, are poorly understood. Here we show that two essential subunits of the basal class I transcription factor A (CITFA) predominantly occupied the promoter of the active BES relative to that of a silent BES, a phenotype that was maintained after switching BESs in situ . In these experiments, high promoter occupancy of CITFA was coupled to high levels of both promoter-proximal RNA abundance and RNA polymerase I occupancy. Accordingly, fluorescently tagged CITFA-7 was concentrated in the nucleolus and the ESB. Because a ChIP-seq analysis found that along the entire BES, CITFA-7 is specifically enriched only at the promoter, our data strongly indicate that monoallelic BES transcription is activated by a mechanism that functions at the level of transcription initiation.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 2
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    Cross-species hybridization of microarrays for studying tumor transcriptome of brain metastasis [Medical Sciences] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-10-19
    Description: Although the importance of the cellular microenvironment (soil) during invasion and metastasis of cancer cells (seed) has been well-recognized, technical challenges have limited the ability to assess the influence of the microenvironment on cancer cells at the molecular level. Here, we show that an experimental strategy, competitive cross-species hybridization of microarray experiments, can characterize the influence of different microenvironments on cancer cells by independently extracting gene expression data of cancer and host cells when human cancer cells were xenografted into different organ sites of immunocompromised mice. Surprisingly, the analysis of gene expression data showed that the brain microenvironment induces complete reprogramming of metastasized cancer cells, resulting in a gain of neuronal cell characteristics and mimicking neurogenesis during development. We also show that epigenetic changes coincide with transcriptional reprogramming in cancer cells. These observations provide proof of principle for competitive cross-species hybridization of microarray experiments to characterize the effect of the microenvironment on tumor cell behavior.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 3
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    Transcriptional regulation in pluripotent stem cells by methyl CpG-binding protein 2 (MeCP2) (2014)
    Oxford University Press
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    Publication Date: 2014-01-24
    Description: Rett syndrome (RTT) is one of the most prevalent female mental disorders. De novo mutations in methyl CpG-binding protein 2 (MeCP2) are a major cause of RTT. MeCP2 regulates gene expression as a transcription regulator as well as through long-range chromatin interaction. Because MeCP2 is present on the X chromosome, RTT is manifested in an X-linked dominant manner. Investigation using murine MeCP2 null models and post-mortem human brain tissues has contributed to understanding the molecular and physiological function of MeCP2. In addition, RTT models using human induced pluripotent stem cells derived from RTT patients (RTT-iPSCs) provide novel resources to elucidate the regulatory mechanism of MeCP2. Previously, we obtained clones of female RTT-iPSCs that express either wild-type or mutant MECP2 due to the inactivation of one X chromosome. Reactivation of the X chromosome also allowed us to have RTT-iPSCs that express both wild-type and mutant MECP2 . Using these unique pluripotent stem cells, we investigated the regulation of gene expression by MeCP2 in pluripotent stem cells by transcriptome analysis. We found that MeCP2 regulates genes encoding mitochondrial membrane proteins. In addition, loss of function in MeCP2 results in de-repression of genes on the inactive X chromosome. Furthermore, we showed that each mutation in MECP2 affects a partly different set of genes. These studies suggest that fundamental cellular physiology is affected by mutations in MECP2 from early development, and that a therapeutic approach targeting to unique forms of mutant MeCP2 is needed.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 4
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    Attenuation of noise-induced hearing loss using methylene blue (2014)
    Springer Nature
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    Publication Date: 2014-04-25
    Description: Attenuation of noise-induced hearing loss using methylene blue Cell Death and Disease 5, e1200 (April 2014). doi:10.1038/cddis.2014.170 Authors: J-S Park, I Jou & S M Park
    Keywords: noise-induced hearing losscochleamitochondrial respiratory chainreactive oxygen speciesmethylene blueneurotrophin-3
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 5
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    CD95 promotes tumour growth (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-05-28
    Description: CD95 (also called Fas and APO-1) is a prototypical death receptor that regulates tissue homeostasis mainly in the immune system through the induction of apoptosis. During cancer progression CD95 is frequently downregulated or cells are rendered apoptosis resistant, raising the possibility that loss of CD95 is part of a mechanism for tumour evasion. However, complete loss of CD95 is rarely seen in human cancers and many cancer cells express large quantities of CD95 and are highly sensitive to CD95-mediated apoptosis in vitro. Furthermore, cancer patients frequently have elevated levels of the physiological ligand for CD95, CD95L. These data raise the possibility that CD95 could actually promote the growth of tumours through its non-apoptotic activities. Here we show that cancer cells in general, regardless of their CD95 apoptosis sensitivity, depend on constitutive activity of CD95, stimulated by cancer-produced CD95L, for optimal growth. Consistently, loss of CD95 in mouse models of ovarian cancer and liver cancer reduces cancer incidence as well as the size of the tumours. The tumorigenic activity of CD95 is mediated by a pathway involving JNK and Jun. These results demonstrate that CD95 has a growth-promoting role during tumorigenesis and indicate that efforts to inhibit its activity rather than to enhance it should be considered during cancer therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879093/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879093/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Lina -- Park, Sun-Mi -- Tumanov, Alexei V -- Hau, Annika -- Sawada, Kenjiro -- Feig, Christine -- Turner, Jerrold R -- Fu, Yang-Xin -- Romero, Iris L -- Lengyel, Ernst -- Peter, Marcus E -- CA112240/CA/NCI NIH HHS/ -- K12 HD000849/HD/NICHD NIH HHS/ -- L30 CA153336/CA/NCI NIH HHS/ -- R01 CA095319/CA/NCI NIH HHS/ -- R01 CA11182/CA/NCI NIH HHS/ -- R01 CA112240/CA/NCI NIH HHS/ -- R01 CA112240-01A1/CA/NCI NIH HHS/ -- R01 CA112240-02/CA/NCI NIH HHS/ -- R01 CA112240-03/CA/NCI NIH HHS/ -- R01 CA112240-04/CA/NCI NIH HHS/ -- R01 CA112240-05/CA/NCI NIH HHS/ -- England -- Nature. 2010 May 27;465(7297):492-6. doi: 10.1038/nature09075.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Ben May Department for Cancer Research, The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20505730" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/deficiency/genetics/*metabolism ; Apoptosis ; Carcinoma, Endometrioid/metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation ; Fas Ligand Protein/antagonists & inhibitors/immunology/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Hepatocytes/enzymology/metabolism/pathology ; Humans ; Liver Neoplasms/enzymology/metabolism/pathology ; Male ; Mice ; Mitogen-Activated Protein Kinase 8/deficiency/genetics/metabolism ; Neoplasms/*metabolism/*pathology ; Ovarian Neoplasms/metabolism/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    The novel gene twenty-four defines a critical translational step in the Drosophila clock (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-02-19
    Description: Daily oscillations of gene expression underlie circadian behaviours in multicellular organisms. While attention has been focused on transcriptional and post-translational mechanisms, other post-transcriptional modes have been less clearly delineated. Here we report mutants of a novel Drosophila gene twenty-four (tyf) that show weak behavioural rhythms. Weak rhythms are accompanied by marked reductions in the levels of the clock protein Period (PER) as well as more modest effects on Timeless (TIM). Nonetheless, PER induction in pacemaker neurons can rescue tyf mutant rhythms. TYF associates with a 5'-cap-binding complex, poly(A)-binding protein (PABP), as well as per and tim transcripts. Furthermore, TYF activates reporter expression when tethered to reporter messenger RNA even in vitro. Taken together, these data indicate that TYF potently activates PER translation in pacemaker neurons to sustain robust rhythms, revealing a new and important role for translational control in the Drosophila circadian clock.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073513/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073513/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, Chunghun -- Lee, Jongbin -- Choi, Changtaek -- Kilman, Valerie L -- Kim, Juwon -- Park, Sung Mi -- Jang, Sung Key -- Allada, Ravi -- Choe, Joonho -- R01 MH067870/MH/NIMH NIH HHS/ -- R01 MH067870-05/MH/NIMH NIH HHS/ -- R01 NS052903/NS/NINDS NIH HHS/ -- R01 NS052903-04/NS/NINDS NIH HHS/ -- R01 NS059042/NS/NINDS NIH HHS/ -- R01 NS059042-04/NS/NINDS NIH HHS/ -- R01MH067870/MH/NIMH NIH HHS/ -- R01NS052903/NS/NINDS NIH HHS/ -- R01NS059042/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Feb 17;470(7334):399-403. doi: 10.1038/nature09728.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21331043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Circadian Clocks/*genetics/physiology ; Circadian Rhythm/genetics/physiology ; Drosophila Proteins/biosynthesis/genetics/*metabolism ; Drosophila melanogaster/*genetics/*physiology ; Genes, Insect/*genetics ; Genes, Reporter/genetics ; Mutation/genetics ; Neurons/metabolism/physiology ; Period Circadian Proteins/*biosynthesis/genetics/metabolism ; Poly(A)-Binding Proteins/metabolism ; Protein Binding ; Protein Biosynthesis/genetics/*physiology ; RNA, Messenger/genetics/metabolism ; Up-Regulation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Investigation of plasma-doped fin structure and characterization of dopants by atom probe tomography (2012)
    American Institute of Physics
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    Publication Date: 2012-11-19
    Print ISSN: 0003-6951
    Electronic ISSN: 1077-3118
    Topics: Physics
    Published by American Institute of Physics
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  • 8
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    Cap-dependent translation without base-by-base scanning of an messenger ribonucleic acid (2012)
    Oxford University Press
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    Publication Date: 2012-08-23
    Description: ‘Ribosome scanning’ is the generally accepted mechanism for explaining how a ribosome finds an initiation codon located far removed from the ribosome recruiting site (cap structure). However, the molecular characteristics of ribosome scanning along 5' untranslated regions (UTRs) remain obscure. Herein, using a rabbit reticulocyte lysate (RRL) system and artificial ribonucleic acid (RNA) constructs composed of a capped leader RNA and an uncapped reporter RNA annealed through a double-stranded RNA (dsRNA) bridge, we show that the ribosome can efficiently bypass a stable, dsRNA region without melting the structure. The insertion of an upstream open reading frame in the capped leader RNA impaired the translation of reporter RNA, indicating that a ribosome associated with the 5'-end explores the regions upstream of the dsRNA bridge in search of the initiation codon. These data indicate that a ribosome may skip part(s) of an messenger RNA 5'UTR without thoroughly scanning it.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 9
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    Analysis on Passivity for Uncertain Neural Networks with Time-Varying Delays (2014)
    Hindawi
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    Publication Date: 2014-06-18
    Description: The problem of passivity analysis for neural networks with time-varying delays and parameter uncertainties is considered. By the consideration of newly constructed Lyapunov-Krasovskii functionals, improved sufficient conditions to guarantee the passivity of the concerned networks are proposed with the framework of linear matrix inequalities (LMIs), which can be solved easily by various efficient convex optimization algorithms. The enhancement of the feasible region of the proposed criteria is shown via two numerical examples by the comparison of maximum allowable delay bounds.
    Print ISSN: 1024-123X
    Electronic ISSN: 1563-5147
    Topics: Mathematics , Technology
    Published by Hindawi
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  • 10
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    CysLTR1 signaling in noise-induced cochlear injury [Medical Sciences] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-07-09
    Description: Noise-induced hearing loss is one of the most common types of sensorineural hearing loss. In this study, we examined the expression and localization of leukotriene receptors and their respective changes in the cochlea after hazardous noise exposure. We found that the expression of cysteinyl leukotriene type 1 receptor (CysLTR1) was...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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