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  • 1
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    Global control of dimorphism and virulence in fungi (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-04-29
    Beschreibung: Microbial pathogens that normally inhabit our environment can adapt to thrive inside mammalian hosts. There are six dimorphic fungi that cause disease worldwide, which switch from nonpathogenic molds in soil to pathogenic yeast after spores are inhaled and exposed to elevated temperature. Mechanisms that regulate this switch remain obscure. We show that a hybrid histidine kinase senses host signals and triggers the transition from mold to yeast. The kinase also regulates cell-wall integrity, sporulation, and expression of virulence genes in vivo. This global regulator shapes how dimorphic fungal pathogens adapt to the mammalian host, which has broad implications for treating and preventing systemic fungal disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemecek, Julie C -- Wuthrich, Marcel -- Klein, Bruce S -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):583-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, University of Wisconsin Hospital and Clinics, Madison, WI 53792, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645097" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blastomyces/cytology/enzymology/*genetics/*pathogenicity ; Blastomycosis/microbiology ; Coccidioides/enzymology/genetics/pathogenicity ; Fungal Proteins/genetics/physiology ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Genetic Complementation Test ; Histoplasma/enzymology/genetics/pathogenicity ; Histoplasmosis/microbiology ; Lung Diseases, Fungal/microbiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutagenesis, Insertional ; Open Reading Frames ; Protein Kinases/chemistry/*genetics/*physiology ; RNA Interference ; Saccharomyces cerevisiae/genetics ; Soil Microbiology ; Spores, Fungal/physiology ; Temperature ; Virulence/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Sequence and structural convergence of broad and potent HIV antibodies that mimic CD4 binding (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2011-07-19
    Beschreibung: Passive transfer of broadly neutralizing HIV antibodies can prevent infection, which suggests that vaccines that elicit such antibodies would be protective. Thus far, however, few broadly neutralizing HIV antibodies that occur naturally have been characterized. To determine whether these antibodies are part of a larger group of related molecules, we cloned 576 new HIV antibodies from four unrelated individuals. All four individuals produced expanded clones of potent broadly neutralizing CD4-binding-site antibodies that mimic binding to CD4. Despite extensive hypermutation, the new antibodies shared a consensus sequence of 68 immunoglobulin H (IgH) chain amino acids and arise independently from two related IgH genes. Comparison of the crystal structure of one of the antibodies to the broadly neutralizing antibody VRC01 revealed conservation of the contacts to the HIV spike.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351836/" 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/PMC3351836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheid, Johannes F -- Mouquet, Hugo -- Ueberheide, Beatrix -- Diskin, Ron -- Klein, Florian -- Oliveira, Thiago Y K -- Pietzsch, John -- Fenyo, David -- Abadir, Alexander -- Velinzon, Klara -- Hurley, Arlene -- Myung, Sunnie -- Boulad, Farid -- Poignard, Pascal -- Burton, Dennis R -- Pereyra, Florencia -- Ho, David D -- Walker, Bruce D -- Seaman, Michael S -- Bjorkman, Pamela J -- Chait, Brian T -- Nussenzweig, Michel C -- P01 AI081677/AI/NIAID NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- R01 AI033292/AI/NIAID NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- RR022220/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1633-7. doi: 10.1126/science.1207227. Epub 2011 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764753" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Antibodies, Neutralizing/*chemistry/*immunology/metabolism ; Antibody Affinity ; Antibody Specificity ; Antigens, CD4/immunology/*metabolism ; Binding Sites ; Binding Sites, Antibody ; Cloning, Molecular ; Consensus Sequence ; Crystallography, X-Ray ; Genes, Immunoglobulin Heavy Chain ; HIV Antibodies/*chemistry/*immunology/metabolism ; HIV Envelope Protein gp120/chemistry/*immunology/metabolism ; HIV Infections/immunology ; Humans ; Immunoglobulin Fab Fragments/chemistry ; Immunoglobulin Heavy Chains/chemistry ; Immunoglobulin Light Chains/chemistry ; Molecular Mimicry ; Molecular Sequence Data ; Mutation ; Protein Conformation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Increasing the potency and breadth of an HIV antibody by using structure-based rational design (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2011-10-29
    Beschreibung: Antibodies against the CD4 binding site (CD4bs) on the HIV-1 spike protein gp120 can show exceptional potency and breadth. We determined structures of NIH45-46, a more potent clonal variant of VRC01, alone and bound to gp120. Comparisons with VRC01-gp120 revealed that a four-residue insertion in heavy chain complementarity-determining region 3 (CDRH3) contributed to increased interaction between NIH45-46 and the gp120 inner domain, which correlated with enhanced neutralization. We used structure-based design to create NIH45-46(G54W), a single substitution in CDRH2 that increases contact with the gp120 bridging sheet and improves breadth and potency, critical properties for potential clinical use, by an order of magnitude. Together with the NIH45-46-gp120 structure, these results indicate that gp120 inner domain and bridging sheet residues should be included in immunogens to elicit CD4bs antibodies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232316/" 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/PMC3232316/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diskin, Ron -- Scheid, Johannes F -- Marcovecchio, Paola M -- West, Anthony P Jr -- Klein, Florian -- Gao, Han -- Gnanapragasam, Priyanthi N P -- Abadir, Alexander -- Seaman, Michael S -- Nussenzweig, Michel C -- Bjorkman, Pamela J -- P01 AI081677-01/AI/NIAID NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- RR022220/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Dec 2;334(6060):1289-93. doi: 10.1126/science.1213782. Epub 2011 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22033520" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): AIDS Vaccines ; Amino Acid Sequence ; Antibodies, Neutralizing/chemistry/*immunology/metabolism ; Antibody Affinity ; Antigens, CD4/chemistry/metabolism ; Binding Sites ; Complementarity Determining Regions ; Crystallography, X-Ray ; HIV Antibodies/chemistry/*immunology/metabolism ; HIV Envelope Protein gp120/chemistry/*immunology/metabolism ; HIV-1/*immunology ; Humans ; Hydrophobic and Hydrophilic Interactions ; Immunoglobulin Fab Fragments/chemistry/immunology/metabolism ; Immunoglobulin Heavy Chains/chemistry/immunology/metabolism ; Molecular Mimicry ; Molecular Sequence Data ; Mutant Proteins/chemistry/immunology/metabolism ; Protein Conformation ; *Protein Engineering ; Protein Structure, Tertiary
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    A secreted PTEN phosphatase that enters cells to alter signaling and survival (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2013-06-08
    Beschreibung: Phosphatase and tensin homolog on chromosome ten (PTEN) is a tumor suppressor and an antagonist of the phosphoinositide-3 kinase (PI3K) pathway. We identified a 576-amino acid translational variant of PTEN, termed PTEN-Long, that arises from an alternative translation start site 519 base pairs upstream of the ATG initiation sequence, adding 173 N-terminal amino acids to the normal PTEN open reading frame. PTEN-Long is a membrane-permeable lipid phosphatase that is secreted from cells and can enter other cells. As an exogenous agent, PTEN-Long antagonized PI3K signaling and induced tumor cell death in vitro and in vivo. By providing a means to restore a functional tumor-suppressor protein to tumor cells, PTEN-Long may have therapeutic uses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3935617/" 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/PMC3935617/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hopkins, Benjamin D -- Fine, Barry -- Steinbach, Nicole -- Dendy, Meaghan -- Rapp, Zachary -- Shaw, Jacquelyn -- Pappas, Kyrie -- Yu, Jennifer S -- Hodakoski, Cindy -- Mense, Sarah -- Klein, Joshua -- Pegno, Sarah -- Sulis, Maria-Luisa -- Goldstein, Hannah -- Amendolara, Benjamin -- Lei, Liang -- Maurer, Matthew -- Bruce, Jeffrey -- Canoll, Peter -- Hibshoosh, Hanina -- Parsons, Ramon -- 2T32 CA09503/CA/NCI NIH HHS/ -- CA082783/CA/NCI NIH HHS/ -- CA097403/CA/NCI NIH HHS/ -- P01 CA097403/CA/NCI NIH HHS/ -- R01 CA082783/CA/NCI NIH HHS/ -- R01 CA155117/CA/NCI NIH HHS/ -- R01 NS066955/NS/NINDS NIH HHS/ -- R01 NS073610/NS/NINDS NIH HHS/ -- R01NS066955/NS/NINDS NIH HHS/ -- T32 CA009503/CA/NCI NIH HHS/ -- T32 GM008224/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Jul 26;341(6144):399-402. doi: 10.1126/science.1234907. Epub 2013 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23744781" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Cell Line, Tumor ; *Cell Survival ; Embryonic Stem Cells ; Glioblastoma/drug therapy/metabolism/pathology ; HEK293 Cells ; Humans ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutation ; PTEN Phosphohydrolase/*chemistry/genetics/*metabolism/pharmacology ; Peptide Chain Initiation, Translational ; Phosphatidylinositol 3-Kinase/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Messenger/genetics/metabolism ; *Signal Transduction/drug effects ; Xenograft Model Antitumor Assays
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Positional cloning of a gene for nematode resistance in sugar beet (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1997-02-07
    Beschreibung: The Hs1(pro-1) locus confers resistance to the beet cyst nematode (Heterodera schachtii Schmidt), a major pest in the cultivation of sugar beet (Beta vulgaris L.). The Hs1(pro-1) gene was cloned with the use of genome-specific satellite markers and chromosomal break-point analysis. Expression of the corresponding complementary DNA in a susceptible sugar beet conferred resistance to infection with the beet cyst nematode. The native Hs1(pro-1) gene, expressed in roots, encodes a 282-amino acid protein with imperfect leucine-rich repeats and a putative membrane-spanning segment, features similar to those of disease resistance genes previously cloned from higher plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cai, D -- Kleine, M -- Kifle, S -- Harloff, H J -- Sandal, N N -- Marcker, K A -- Klein-Lankhorst, R M -- Salentijn, E M -- Lange, W -- Stiekema, W J -- Wyss, U -- Grundler, F M -- Jung, C -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):832-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Crop Science and Plant Breeding, Christian-Albrechts-University of Kiel, Olshausenstrasse 40, D-24118 Kiel, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9012350" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Cell Membrane/chemistry ; *Cloning, Molecular ; DNA, Complementary/genetics ; *Genes, Plant ; Genetic Complementation Test ; Leucine/chemistry ; Membrane Proteins/chemistry/*genetics/physiology ; Molecular Sequence Data ; Nematoda/*pathogenicity ; Plant Diseases/*genetics/parasitology ; *Plant Proteins ; Plant Roots/genetics/parasitology ; Transformation, Genetic ; Vegetables/*genetics/*parasitology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Obestatin, a peptide encoded by the ghrelin gene, opposes ghrelin's effects on food intake (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2005-11-15
    Beschreibung: Ghrelin, a circulating appetite-inducing hormone, is derived from a prohormone by posttranslational processing. On the basis of the bioinformatic prediction that another peptide also derived from proghrelin exists, we isolated a hormone from rat stomach and named it obestatin-a contraction of obese, from the Latin "obedere," meaning to devour, and "statin," denoting suppression. Contrary to the appetite-stimulating effects of ghrelin, treatment of rats with obestatin suppressed food intake, inhibited jejunal contraction, and decreased body-weight gain. Obestatin bound to the orphan G protein-coupled receptor GPR39. Thus, two peptide hormones with opposing action in weight regulation are derived from the same ghrelin gene. After differential modification, these hormones activate distinct receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jian V -- Ren, Pei-Gen -- Avsian-Kretchmer, Orna -- Luo, Ching-Wei -- Rauch, Rami -- Klein, Cynthia -- Hsueh, Aaron J W -- New York, N.Y. -- Science. 2005 Nov 11;310(5750):996-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Reproductive Biology, Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, CA 94305-5317, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16284174" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; CHO Cells ; Computational Biology ; Conserved Sequence ; Cricetinae ; *Eating/drug effects ; Fasting ; Gastric Emptying/drug effects ; Gastrointestinal Motility/drug effects ; Ghrelin ; Humans ; In Vitro Techniques ; Ligands ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Peptide Hormones/blood/chemistry/*genetics/metabolism/pharmacology/*physiology ; Protein Binding ; Protein Precursors/*genetics ; Radioimmunoassay ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Ghrelin ; Signal Transduction ; Weight Gain/drug effects
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Antibody-mediated immunotherapy of macaques chronically infected with SHIV suppresses viraemia (2013)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2013-11-01
    Beschreibung: Neutralizing antibodies can confer immunity to primate lentiviruses by blocking infection in macaque models of AIDS. However, earlier studies of anti-human immunodeficiency virus type 1 (HIV-1) neutralizing antibodies administered to infected individuals or humanized mice reported poor control of virus replication and the rapid emergence of resistant variants. A new generation of anti-HIV-1 monoclonal antibodies, possessing extraordinary potency and breadth of neutralizing activity, has recently been isolated from infected individuals. These neutralizing antibodies target different regions of the HIV-1 envelope glycoprotein including the CD4-binding site, glycans located in the V1/V2, V3 and V4 regions, and the membrane proximal external region of gp41 (refs 9-14). Here we have examined two of the new antibodies, directed to the CD4-binding site and the V3 region (3BNC117 and 10-1074, respectively), for their ability to block infection and suppress viraemia in macaques infected with the R5 tropic simian-human immunodeficiency virus (SHIV)-AD8, which emulates many of the pathogenic and immunogenic properties of HIV-1 during infections of rhesus macaques. Either antibody alone can potently block virus acquisition. When administered individually to recently infected macaques, the 10-1074 antibody caused a rapid decline in virus load to undetectable levels for 4-7 days, followed by virus rebound during which neutralization-resistant variants became detectable. When administered together, a single treatment rapidly suppressed plasma viraemia for 3-5 weeks in some long-term chronically SHIV-infected animals with low CD4(+) T-cell levels. A second cycle of anti-HIV-1 monoclonal antibody therapy, administered to two previously treated animals, successfully controlled virus rebound. These results indicate that immunotherapy or a combination of immunotherapy plus conventional antiretroviral drugs might be useful as a treatment for chronically HIV-1-infected individuals experiencing immune dysfunction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133787/" 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/PMC4133787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shingai, Masashi -- Nishimura, Yoshiaki -- Klein, Florian -- Mouquet, Hugo -- Donau, Olivia K -- Plishka, Ronald -- Buckler-White, Alicia -- Seaman, Michael -- Piatak, Michael Jr -- Lifson, Jeffrey D -- Dimitrov, Dimiter S -- Nussenzweig, Michel C -- Martin, Malcolm A -- HHSN261200800001E/PHS HHS/ -- P01 AI100148/AI/NIAID NIH HHS/ -- ZIA AI000415-29/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Nov 14;503(7475):277-80. doi: 10.1038/nature12746. Epub 2013 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24172896" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies, Neutralizing/*therapeutic use ; Antigens, CD4/metabolism ; Binding Sites/immunology ; HIV Antibodies/*therapeutic use ; HIV Envelope Protein gp120/immunology ; HIV-1/*immunology ; *Immunotherapy ; Macaca/immunology ; Molecular Sequence Data ; Peptide Fragments/immunology ; Simian Acquired Immunodeficiency Syndrome/prevention & control/*therapy ; Simian Immunodeficiency Virus/*physiology ; Time Factors ; Viral Load ; Viremia/*therapy
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    A novel ChREBP isoform in adipose tissue regulates systemic glucose metabolism (2012)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2012-04-03
    Beschreibung: The prevalence of obesity and type 2 diabetes is increasing worldwide and threatens to shorten lifespan. Impaired insulin action in peripheral tissues is a major pathogenic factor. Insulin stimulates glucose uptake in adipose tissue through the GLUT4 (also known as SLC2A4) glucose transporter, and alterations in adipose tissue GLUT4 expression or function regulate systemic insulin sensitivity. Downregulation of human and mouse adipose tissue GLUT4 occurs early in diabetes development. Here we report that adipose tissue GLUT4 regulates the expression of carbohydrate-responsive-element-binding protein (ChREBP; also known as MLXIPL), a transcriptional regulator of lipogenic and glycolytic genes. Furthermore, adipose ChREBP is a major determinant of adipose tissue fatty acid synthesis and systemic insulin sensitivity. We find a new mechanism for glucose regulation of ChREBP: glucose-mediated activation of the canonical ChREBP isoform (ChREBP-alpha) induces expression of a novel, potent isoform (ChREBP-beta) that is transcribed from an alternative promoter. ChREBP-beta expression in human adipose tissue predicts insulin sensitivity, indicating that it may be an effective target for treating diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341994/" 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/PMC3341994/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herman, Mark A -- Peroni, Odile D -- Villoria, Jorge -- Schon, Michael R -- Abumrad, Nada A -- Bluher, Matthias -- Klein, Samuel -- Kahn, Barbara B -- DK037948/DK/NIDDK NIH HHS/ -- DK046200/DK/NIDDK NIH HHS/ -- DK056341/DK/NIDDK NIH HHS/ -- DK057521/DK/NIDDK NIH HHS/ -- K08 DK076726/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-11/DK/NIDDK NIH HHS/ -- R01 DK037948/DK/NIDDK NIH HHS/ -- R01 DK037948-22/DK/NIDDK NIH HHS/ -- R01 DK098002/DK/NIDDK NIH HHS/ -- R37 DK043051/DK/NIDDK NIH HHS/ -- R37 DK43051/DK/NIDDK NIH HHS/ -- England -- Nature. 2012 Apr 19;484(7394):333-8. doi: 10.1038/nature10986.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22466288" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipocytes/metabolism ; Adipose Tissue/cytology/*metabolism/pathology ; Adiposity ; Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription ; Factors/chemistry/genetics/*metabolism ; Blood Glucose/metabolism ; Body Mass Index ; Body Weight ; Cells, Cultured ; Cohort Studies ; Cross-Sectional Studies ; Diabetes Mellitus/blood/genetics/metabolism ; Female ; Gene Expression Regulation/genetics ; Genotype ; Glucose/*metabolism/pharmacology ; Glucose Intolerance/genetics ; Glucose Transporter Type 4/biosynthesis/genetics/metabolism ; Homeostasis/genetics ; Humans ; Insulin/metabolism/pharmacology ; Insulin Resistance/genetics ; Lipogenesis ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Nuclear Proteins/chemistry/deficiency/genetics/*metabolism ; Obesity/genetics/metabolism ; Promoter Regions, Genetic/genetics ; Protein Isoforms/chemistry/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Transcription Factors/chemistry/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Increased recruitment of TATA-binding protein to the promoter by transcriptional activation domains in vivo (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-10-14
    Beschreibung: The rate at which the TATA-binding protein (TBP) interacts with the TATA element and promotes transcription by RNA polymerase II was determined in yeast cells. A TBP derivative with altered TATA-element specificity was rapidly induced, and transcription from promoters with appropriately mutated TATA elements was measured. Without a functional activator protein, basal transcription was observed only after a lag of several hours. In contrast, GCN4-activated transcription occurred rapidly upon induction of the TBP derivative. These results suggest that accessibility of TBP to the chromatin template in vivo is rate limiting and that activation domains increase recruitment of TBP to the promoter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klein, C -- Struhl, K -- GM30186/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):280-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939664" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Base Sequence ; Binding Sites ; Chromatin/metabolism ; Copper/pharmacology ; DNA-Binding Proteins/*metabolism ; Fungal Proteins/metabolism/pharmacology ; Hydro-Lyases/genetics ; Molecular Sequence Data ; Protein Kinases/metabolism/pharmacology ; *Saccharomyces cerevisiae Proteins ; *TATA Box ; TATA-Box Binding Protein ; Templates, Genetic ; Transcription Factors/*metabolism/pharmacology ; *Transcriptional Activation ; Yeasts/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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    Induction of mesoderm in Xenopus laevis embryos by translation initiation factor 4E (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-08-05
    Beschreibung: The microinjection of messenger RNA encoding the eukaryotic translation initiation factor 4E (eIF-4E) into early embryos of Xenopus laevis leads to the induction of mesoderm in ectodermal explants. This induction occurs without a stimulation of overall protein synthesis and is blocked by the co-expression of a dominant negative mutant of the proto-oncogene ras or a truncated activin type II receptor. Although other translation factors have been studied in vertebrate and invertebrate embryos, none have been shown to play a direct role in development. The results here suggest a mechanism for relaying and amplifying signals for mesoderm induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klein, P S -- Melton, D A -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):803-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047887" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Sequence ; Eukaryotic Initiation Factor-1/physiology ; Eukaryotic Initiation Factor-4E ; Gene Expression Regulation/physiology ; Mesoderm/metabolism/*physiology ; Molecular Sequence Data ; Peptide Initiation Factors/genetics/*physiology ; RNA, Messenger ; Xenopus laevis/*embryology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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