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  • Humans  (11)
  • Male  (4)
  • American Association for the Advancement of Science (AAAS)  (11)
  • 1
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    Divergent regulation of dihydrofolate reductase between malaria parasite and human host (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-20
    Description: For half a century, successful antifolate therapy against Plasmodium falciparum malaria has been attributed to host-parasite differences in drug binding to dihydrofolate reductase-thymidylate synthase (DHFR-TS). Selectivity may also arise through previously unappreciated differences in regulation of this drug target. The DHFR-TS of Plasmodium binds its cognate messenger RNA (mRNA) and inhibits its own translation. However, unlike translational regulation of DHFR or TS in humans, DHFR-TS mRNA binding is not coupled to enzyme active sites. Thus, antifolate treatment does not relieve translational inhibition and parasites cannot replenish dead enzyme.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830934/" 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/PMC3830934/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Kai -- Rathod, Pradipsinh K -- AI26912/AI/NIAID NIH HHS/ -- AI40956/AI/NIAID NIH HHS/ -- R01 AI026912/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 19;296(5567):545-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, The Catholic University of America, Washington, DC 20064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11964483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimalarials/pharmacology ; Catalytic Domain ; Cell Line ; Folic Acid Antagonists/*pharmacology ; Host-Parasite Interactions ; Humans ; Multienzyme Complexes/chemistry/*genetics/*metabolism ; Plasmodium falciparum/*enzymology/genetics ; Protein Biosynthesis ; RNA, Messenger/genetics/metabolism ; RNA, Protozoan/genetics/metabolism ; Recombinant Proteins/genetics/metabolism ; Tetrahydrofolate Dehydrogenase/chemistry/*genetics/*metabolism ; Thymidylate Synthase/chemistry/*genetics/*metabolism ; Triazines/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Adenovirus small e1a alters global patterns of histone modification (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-23
    Description: Adenovirus small early region 1a (e1a) protein drives cells into S phase by binding RB family proteins and the closely related histone acetyl transferases p300 and CBP. The interaction with RB proteins displaces them from DNA-bound E2F transcription factors, reversing their repression of cell cycle genes. However, it has been unclear how the e1a interaction with p300 and CBP promotes passage through the cell cycle. We show that this interaction causes a threefold reduction in total cellular histone H3 lysine 18 acetylation (H3K18ac). CBP and p300 are required for acetylation at this site because their knockdown causes specific hypoacetylation at H3K18. SV40 T antigen also induces H3K18 hypoacetylation. Because global hypoacetylation at this site is observed in prostate carcinomas with poor prognosis, this suggests that processes resulting in global H3K18 hypoacetylation may be linked to oncogenic transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756290/" 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/PMC2756290/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horwitz, Gregory A -- Zhang, Kangling -- McBrian, Matthew A -- Grunstein, Michael -- Kurdistani, Siavash K -- Berk, Arnold J -- CA25235/CA/NCI NIH HHS/ -- R37 CA025235/CA/NCI NIH HHS/ -- R37 CA025235-30/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1084-5. doi: 10.1126/science.1155544.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719283" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Adenovirus E1A Proteins/genetics/*metabolism ; Adenoviruses, Human/*metabolism ; Antigens, Polyomavirus Transforming/metabolism ; CREB-Binding Protein/metabolism ; *Cell Cycle ; Cell Line ; Cell Transformation, Viral ; Cells, Cultured ; HeLa Cells ; Histones/*metabolism ; Humans ; Lysine/metabolism ; Mutation ; p300-CBP Transcription Factors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    A mutation in EGF repeat-8 of Notch discriminates between Serrate/Jagged and Delta family ligands (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-01
    Description: Notch signaling affects many developmental and cellular processes and has been implicated in congenital disorders, stroke, and numerous cancers. The Notch receptor binds its ligands Delta and Serrate and is able to discriminate between them in different contexts. However, the specific domains in Notch responsible for this selectivity are poorly defined. Through genetic screens in Drosophila, we isolated a mutation, Notch(jigsaw), that affects Serrate- but not Delta-dependent signaling. Notch(jigsaw) carries a missense mutation in epidermal growth factor repeat-8 (EGFr-8) and is defective in Serrate binding. A homologous point mutation in mammalian Notch2 also exhibits defects in signaling of a mammalian Serrate homolog, Jagged1. Hence, an evolutionarily conserved valine in EGFr-8 is essential for ligand selectivity and provides a molecular handle to study numerous Notch-dependent signaling events.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3663443/" 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/PMC3663443/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, Shinya -- Charng, Wu-Lin -- Rana, Nadia A -- Kakuda, Shinako -- Jaiswal, Manish -- Bayat, Vafa -- Xiong, Bo -- Zhang, Ke -- Sandoval, Hector -- David, Gabriela -- Wang, Hao -- Haltiwanger, Robert S -- Bellen, Hugo J -- 1RC4GM096355-01/GM/NIGMS NIH HHS/ -- 5K12GM084897/GM/NIGMS NIH HHS/ -- 5P30HD024064/HD/NICHD NIH HHS/ -- 5R01GM061126-12/GM/NIGMS NIH HHS/ -- 5R01GM067858/GM/NIGMS NIH HHS/ -- 5T32-HD055200/HD/NICHD NIH HHS/ -- K12 GM084897/GM/NIGMS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- R01 GM061126/GM/NIGMS NIH HHS/ -- R01 GM067858/GM/NIGMS NIH HHS/ -- RC4 GM096355/GM/NIGMS NIH HHS/ -- T32 HD055200/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1229-32. doi: 10.1126/science.1228745.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Developmental Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23197537" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Calcium-Binding Proteins/*metabolism ; Cells, Cultured ; DNA Mutational Analysis ; Drosophila Proteins/*genetics/*metabolism ; Drosophila melanogaster/genetics/*metabolism ; Epidermal Growth Factor/genetics ; Evolution, Molecular ; Humans ; Intercellular Signaling Peptides and Proteins/*metabolism ; Intracellular Signaling Peptides and Proteins/*metabolism ; Ligands ; Male ; Membrane Proteins/*metabolism ; Methionine/genetics ; Molecular Sequence Data ; Mutation ; Receptor, Notch2/genetics/metabolism ; Receptors, Notch/*genetics/*metabolism ; Tandem Repeat Sequences/genetics ; Valine/genetics ; X Chromosome/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-21
    Description: Age-related macular degeneration (AMD) is the most common cause of irreversible vision loss in the developed world and has a strong genetic predisposition. A locus at human chromosome 10q26 affects the risk of AMD, but the precise gene(s) have not been identified. We genotyped 581 AMD cases and 309 normal controls in a Caucasian cohort in Utah. We demonstrate that a single-nucleotide polymorphism, rs11200638, in the promoter region of HTRA1 is the most likely causal variant for AMD at 10q26 and is estimated to confer a population attributable risk of 49.3%. The HTRA1 gene encodes a secreted serine protease. Preliminary analysis of lymphocytes and retinal pigment epithelium from four AMD patients revealed that the risk allele was associated with elevated expression levels of HTRA1 mRNA and protein. We also found that drusen in the eyes of AMD patients were strongly immunolabeled with HTRA1 antibody. Together, these findings support a key role for HTRA1 in AMD susceptibility and identify a potential new pathway for AMD pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Zhenglin -- Camp, Nicola J -- Sun, Hui -- Tong, Zongzhong -- Gibbs, Daniel -- Cameron, D Joshua -- Chen, Haoyu -- Zhao, Yu -- Pearson, Erik -- Li, Xi -- Chien, Jeremy -- Dewan, Andrew -- Harmon, Jennifer -- Bernstein, Paul S -- Shridhar, Viji -- Zabriskie, Norman A -- Hoh, Josephine -- Howes, Kimberly -- Zhang, Kang -- CA98364/CA/NCI NIH HHS/ -- GCRC M01-RR00064/RR/NCRR NIH HHS/ -- P30EY014800/EY/NEI NIH HHS/ -- R01EY14428/EY/NEI NIH HHS/ -- R01EY14448/EY/NEI NIH HHS/ -- R01EY15771/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):992-3. Epub 2006 Oct 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology and Visual Sciences, Moran Eye Center, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053109" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aging ; Alleles ; Case-Control Studies ; Chromosomes, Human, Pair 10/genetics ; Cohort Studies ; European Continental Ancestry Group/genetics ; Female ; *Genetic Predisposition to Disease ; Genotype ; Homozygote ; Humans ; Lymphocytes/enzymology ; Macular Degeneration/*genetics ; Male ; Middle Aged ; Pigment Epithelium of Eye/enzymology ; *Polymorphism, Single Nucleotide ; *Promoter Regions, Genetic ; RNA, Messenger/genetics/metabolism ; Retinal Drusen/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Serine Endopeptidases/analysis/*genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    A whole-genome association study of major determinants for host control of HIV-1 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-21
    Description: Understanding why some people establish and maintain effective control of HIV-1 and others do not is a priority in the effort to develop new treatments for HIV/AIDS. Using a whole-genome association strategy, we identified polymorphisms that explain nearly 15% of the variation among individuals in viral load during the asymptomatic set-point period of infection. One of these is found within an endogenous retroviral element and is associated with major histocompatibility allele human leukocyte antigen (HLA)-B*5701, whereas a second is located near the HLA-C gene. An additional analysis of the time to HIV disease progression implicated two genes, one of which encodes an RNA polymerase I subunit. These findings emphasize the importance of studying human genetic variation as a guide to combating infectious agents.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1991296/" 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/PMC1991296/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fellay, Jacques -- Shianna, Kevin V -- Ge, Dongliang -- Colombo, Sara -- Ledergerber, Bruno -- Weale, Mike -- Zhang, Kunlin -- Gumbs, Curtis -- Castagna, Antonella -- Cossarizza, Andrea -- Cozzi-Lepri, Alessandro -- De Luca, Andrea -- Easterbrook, Philippa -- Francioli, Patrick -- Mallal, Simon -- Martinez-Picado, Javier -- Miro, Jose M -- Obel, Niels -- Smith, Jason P -- Wyniger, Josiane -- Descombes, Patrick -- Antonarakis, Stylianos E -- Letvin, Norman L -- McMichael, Andrew J -- Haynes, Barton F -- Telenti, Amalio -- Goldstein, David B -- G0200585/Medical Research Council/United Kingdom -- MC_U137884177/Medical Research Council/United Kingdom -- U19 AI067854/AI/NIAID NIH HHS/ -- U19 AI067854-03/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 17;317(5840):944-7. Epub 2007 Jul 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Population Genomics and Pharmacogenetics, Duke Institute for Genome Sciences and Policy, Duke University, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641165" target="_blank"〉PubMed〈/a〉
    Keywords: Cohort Studies ; DNA-Binding Proteins/genetics ; Disease Progression ; Female ; Genes, MHC Class I ; *Genome, Human ; HIV Infections/*genetics/immunology/therapy/*virology ; HIV-1/*physiology ; HLA-B Antigens/*genetics ; HLA-C Antigens/*genetics ; Haplotypes ; Humans ; Immediate-Early Proteins/genetics ; Major Histocompatibility Complex/*genetics ; Male ; Polymorphism, Single Nucleotide ; RNA, Untranslated ; Regression Analysis ; Viral Load
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Genome-wide identification of human RNA editing sites by parallel DNA capturing and sequencing (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: Adenosine-to-inosine (A-to-I) RNA editing leads to transcriptome diversity and is important for normal brain function. To date, only a handful of functional sites have been identified in mammals. We developed an unbiased assay to screen more than 36,000 computationally predicted nonrepetitive A-to-I sites using massively parallel target capture and DNA sequencing. A comprehensive set of several hundred human RNA editing sites was detected by comparing genomic DNA with RNAs from seven tissues of a single individual. Specificity of our profiling was supported by observations of enrichment with known features of targets of adenosine deaminases acting on RNA (ADAR) and validation by means of capillary sequencing. This efficient approach greatly expands the repertoire of RNA editing targets and can be applied to studies involving RNA editing-related human diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Jin Billy -- Levanon, Erez Y -- Yoon, Jung-Ki -- Aach, John -- Xie, Bin -- Leproust, Emily -- Zhang, Kun -- Gao, Yuan -- Church, George M -- New York, N.Y. -- Science. 2009 May 29;324(5931):1210-3. doi: 10.1126/science.1170995.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478186" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/metabolism ; Adrenal Glands/metabolism ; Alu Elements ; Animals ; Base Sequence ; Brain/*metabolism ; DNA/*genetics ; DNA, Complementary ; *Genome, Human ; Humans ; Intestine, Small/metabolism ; Mice ; *RNA Editing ; RNA, Double-Stranded/chemistry/genetics/metabolism ; RNA, Messenger/chemistry/genetics/*metabolism ; RNA-Binding Proteins ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    ER stress controls iron metabolism through induction of hepcidin (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-15
    Description: Hepcidin is a peptide hormone that is secreted by the liver and controls body iron homeostasis. Hepcidin overproduction causes anemia of inflammation, whereas its deficiency leads to hemochromatosis. Inflammation and iron are known extracellular stimuli for hepcidin expression. We found that endoplasmic reticulum (ER) stress also induces hepcidin expression and causes hypoferremia and spleen iron sequestration in mice. CREBH (cyclic AMP response element-binding protein H), an ER stress-activated transcription factor, binds to and transactivates the hepcidin promoter. Hepcidin induction in response to exogenously administered toxins or accumulation of unfolded protein in the ER is defective in CREBH knockout mice, indicating a role for CREBH in ER stress-regulated hepcidin expression. The regulation of hepcidin by ER stress links the intracellular response involved in protein quality control to innate immunity and iron homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923557/" 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/PMC2923557/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vecchi, Chiara -- Montosi, Giuliana -- Zhang, Kezhong -- Lamberti, Igor -- Duncan, Stephen A -- Kaufman, Randal J -- Pietrangelo, Antonello -- DK42394/DK/NIDDK NIH HHS/ -- HL52173/HL/NHLBI NIH HHS/ -- P01 HL057346/HL/NHLBI NIH HHS/ -- P01 HL057346-11A18575/HL/NHLBI NIH HHS/ -- P01 HL057346-128575/HL/NHLBI NIH HHS/ -- R01 HL052173/HL/NHLBI NIH HHS/ -- R01 HL052173-11/HL/NHLBI NIH HHS/ -- R01 HL052173-12/HL/NHLBI NIH HHS/ -- R01 HL052173-12W1/HL/NHLBI NIH HHS/ -- R01 HL052173-13/HL/NHLBI NIH HHS/ -- R03 MH089782/MH/NIMH NIH HHS/ -- R03 MH089782-02/MH/NIMH NIH HHS/ -- R37 DK042394/DK/NIDDK NIH HHS/ -- R37 DK042394-12/DK/NIDDK NIH HHS/ -- R37 DK042394-12S1/DK/NIDDK NIH HHS/ -- R37 DK042394-13/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Aug 14;325(5942):877-80. doi: 10.1126/science.1176639.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Hemochromatosis, Department of Internal Medicine, University Hospital Policlinico di Modena, Modena, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19679815" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antimicrobial Cationic Peptides/*genetics/*metabolism ; Cell Line, Tumor ; Cyclic AMP Response Element-Binding Protein/*metabolism ; Endoplasmic Reticulum/*physiology ; Hepcidins ; Homeostasis ; Humans ; Immunity, Innate ; Iron/blood/*metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; Mutation ; Promoter Regions, Genetic ; Protein Folding ; RNA Interference ; Spleen/metabolism ; *Stress, Physiological ; Transcriptional Activation
    Print ISSN: 0036-8075
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  • 8
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    Tet-mediated formation of 5-carboxylcytosine and its excision by TDG in mammalian DNA (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-06
    Description: The prevalent DNA modification in higher organisms is the methylation of cytosine to 5-methylcytosine (5mC), which is partially converted to 5-hydroxymethylcytosine (5hmC) by the Tet (ten eleven translocation) family of dioxygenases. Despite their importance in epigenetic regulation, it is unclear how these cytosine modifications are reversed. Here, we demonstrate that 5mC and 5hmC in DNA are oxidized to 5-carboxylcytosine (5caC) by Tet dioxygenases in vitro and in cultured cells. 5caC is specifically recognized and excised by thymine-DNA glycosylase (TDG). Depletion of TDG in mouse embyronic stem cells leads to accumulation of 5caC to a readily detectable level. These data suggest that oxidation of 5mC by Tet proteins followed by TDG-mediated base excision of 5caC constitutes a pathway for active DNA demethylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462231/" 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/PMC3462231/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yu-Fei -- Li, Bin-Zhong -- Li, Zheng -- Liu, Peng -- Wang, Yang -- Tang, Qingyu -- Ding, Jianping -- Jia, Yingying -- Chen, Zhangcheng -- Li, Lin -- Sun, Yan -- Li, Xiuxue -- Dai, Qing -- Song, Chun-Xiao -- Zhang, Kangling -- He, Chuan -- Xu, Guo-Liang -- 1S10RR027643-01/RR/NCRR NIH HHS/ -- GM071440/GM/NIGMS NIH HHS/ -- R01 GM071440/GM/NIGMS NIH HHS/ -- S10 RR027643/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1303-7. doi: 10.1126/science.1210944. Epub 2011 Aug 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Group of DNA Metabolism, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21817016" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells ; HEK293 Cells ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; RNA, Small Interfering ; Thymine DNA Glycosylase/genetics/*metabolism ; Transfection
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  • 9
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    Specific and nonhepatotoxic degradation of nuclear hepatitis B virus cccDNA (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-02-22
    Description: Current antiviral agents can control but not eliminate hepatitis B virus (HBV), because HBV establishes a stable nuclear covalently closed circular DNA (cccDNA). Interferon-alpha treatment can clear HBV but is limited by systemic side effects. We describe how interferon-alpha can induce specific degradation of the nuclear viral DNA without hepatotoxicity and propose lymphotoxin-beta receptor activation as a therapeutic alternative. Interferon-alpha and lymphotoxin-beta receptor activation up-regulated APOBEC3A and APOBEC3B cytidine deaminases, respectively, in HBV-infected cells, primary hepatocytes, and human liver needle biopsies. HBV core protein mediated the interaction with nuclear cccDNA, resulting in cytidine deamination, apurinic/apyrimidinic site formation, and finally cccDNA degradation that prevented HBV reactivation. Genomic DNA was not affected. Thus, inducing nuclear deaminases-for example, by lymphotoxin-beta receptor activation-allows the development of new therapeutics that, in combination with existing antivirals, may cure hepatitis B.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lucifora, Julie -- Xia, Yuchen -- Reisinger, Florian -- Zhang, Ke -- Stadler, Daniela -- Cheng, Xiaoming -- Sprinzl, Martin F -- Koppensteiner, Herwig -- Makowska, Zuzanna -- Volz, Tassilo -- Remouchamps, Caroline -- Chou, Wen-Min -- Thasler, Wolfgang E -- Huser, Norbert -- Durantel, David -- Liang, T Jake -- Munk, Carsten -- Heim, Markus H -- Browning, Jeffrey L -- Dejardin, Emmanuel -- Dandri, Maura -- Schindler, Michael -- Heikenwalder, Mathias -- Protzer, Ulrike -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1221-8. doi: 10.1126/science.1243462. Epub 2014 Feb 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Virology, Technische Universitat Munchen-Helmholtz Zentrum Munchen, 81675 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24557838" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antiviral Agents/*pharmacology/therapeutic use ; Cell Line ; Cell Nucleus/virology ; Cytidine/metabolism ; Cytidine Deaminase/biosynthesis ; DNA, Circular/*metabolism ; DNA, Viral/*metabolism ; Hepatitis B/*drug therapy ; Hepatitis B virus/*drug effects/metabolism ; Hepatocytes/*drug effects/metabolism/virology ; Humans ; Interferon-alpha/*pharmacology/therapeutic use ; Liver/drug effects/metabolism/virology ; Lymphotoxin beta Receptor/*agonists/antagonists & inhibitors ; Mice, SCID ; Proteins ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    The structure of the dynactin complex and its interaction with dynein (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-03-31
    Description: Dynactin is an essential cofactor for the microtubule motor cytoplasmic dynein-1. We report the structure of the 23-subunit dynactin complex by cryo-electron microscopy to 4.0 angstroms. Our reconstruction reveals how dynactin is built around a filament containing eight copies of the actin-related protein Arp1 and one of beta-actin. The filament is capped at each end by distinct protein complexes, and its length is defined by elongated peptides that emerge from the alpha-helical shoulder domain. A further 8.2 angstrom structure of the complex between dynein, dynactin, and the motility-inducing cargo adaptor Bicaudal-D2 shows how the translational symmetry of the dynein tail matches that of the dynactin filament. The Bicaudal-D2 coiled coil runs between dynein and dynactin to stabilize the mutually dependent interactions between all three components.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413427/" 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/PMC4413427/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Urnavicius, Linas -- Zhang, Kai -- Diamant, Aristides G -- Motz, Carina -- Schlager, Max A -- Yu, Minmin -- Patel, Nisha A -- Robinson, Carol V -- Carter, Andrew P -- 100387/Wellcome Trust/United Kingdom -- MC_UP_A025_1011/Medical Research Council/United Kingdom -- WT100387/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2015 Mar 27;347(6229):1441-6. doi: 10.1126/science.aaa4080. Epub 2015 Feb 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Division of Structural Studies, Francis Crick Avenue, Cambridge CB2 0QH, UK. ; Department of Chemistry, Physical and Theoretical Chemistry Laboratory, University of Oxford, Oxford OX1 3QZ, UK. ; Medical Research Council Laboratory of Molecular Biology, Division of Structural Studies, Francis Crick Avenue, Cambridge CB2 0QH, UK. cartera@mrc-lmb.cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25814576" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry ; Animals ; Cryoelectron Microscopy ; Dyneins/*chemistry ; Humans ; Mice ; Microtubule-Associated Proteins/*chemistry ; Multiprotein Complexes/*chemistry ; Protein Interaction Mapping ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits/chemistry ; Swine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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