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  • 1
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    Identification of the meiotic life cycle stage of Trypanosoma brucei in the tsetse fly [Genetics] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-03-02
    Description: Elucidating the mechanism of genetic exchange is fundamental for understanding how genes for such traits as virulence, disease phenotype, and drug resistance are transferred between pathogen strains. Genetic exchange occurs in the parasitic protists Trypanosoma brucei, T. cruzi, and Leishmania major, but the precise cellular mechanisms are unknown, because the process has not been observed directly. Here we exploit the identification of homologs of meiotic genes in the T. brucei genome and demonstrate that three functionally distinct, meiosis-specific proteins are expressed in the nucleus of a single specific cell type, defining a previously undescribed developmental stage occurring within the tsetse fly salivary gland. Expression occurs in clonal and mixed infections, indicating that the meiotic program is an intrinsic but hitherto cryptic part of the developmental cycle of trypanosomes. In experimental crosses, expression of meiosis-specific proteins usually occurred before cell fusion. This is evidence of conventional meiotic division in an excavate protist, and the functional conservation of the meiotic machinery in these divergent organisms underlines the ubiquity and basal evolution of meiosis in eukaryotes.
    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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  • 2
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    Coordinate linkage of HIV evolution reveals regions of immunological vulnerability [Chemistry] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-07-13
    Description: Cellular immune control of HIV is mediated, in part, by induction of single amino acid mutations that reduce viral fitness, but compensatory mutations limit this effect. Here, we sought to determine if higher order constraints on viral evolution exist, because some coordinately linked combinations of mutations may hurt viability. Immune targeting of multiple sites in such a multidimensionally conserved region might render the virus particularly vulnerable, because viable escape pathways would be greatly restricted. We analyzed available HIV sequences using a method from physics to reveal distinct groups of amino acids whose mutations are collectively coordinated (“HIV sectors”). From the standpoint of mutations at individual sites, one such group in Gag is as conserved as other collectively coevolving groups of sites in Gag. However, it exhibits higher order conservation indicating constraints on the viability of viral strains with multiple mutations. Mapping amino acids from this group onto protein structures shows that combined mutations likely destabilize multiprotein structural interactions critical for viral function. Persons who durably control HIV without medications preferentially target the sector in Gag predicted to be most vulnerable. By sequencing circulating viruses from these individuals, we find that individual mutations occur with similar frequency in this sector as in other targeted Gag sectors. However, multiple mutations within this sector are very rare, indicating previously unrecognized multidimensional constraints on HIV evolution. Targeting such regions with higher order evolutionary constraints provides a novel approach to immunogen design for a vaccine against HIV and other rapidly mutating viruses.
    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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    A short RNA stem-loop is necessary and sufficient for repression of gene expression during early logarithmic phase in trypanosomes (2014)
    Oxford University Press
    Details
    Publication Date: 2014-06-21
    Description: We have compared the transcriptomes of cultured procyclic Trypanosoma brucei cells in early and late logarithmic phases and found that ~200 mRNAs were differentially regulated. In late log phase cells, the most upregulated mRNA encoded the nucleobase transporter NT8. The 3' untranslated region (UTR) of NT8 contains a short stem–loop cis -element that is necessary for the regulation of NT8 expression in response to external purine levels. When placed in the 3'-UTR of an unregulated transcript, the cis -element is sufficient to confer regulation in response to purines. To our knowledge, this is the first example of a discrete RNA element that can autonomously regulate gene expression in trypanosomes in response to an external factor and reveals an unprecedented purine-dependent signaling pathway that controls gene expression in eukaryotes.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 4
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    Elevated HLA-A expression impairs HIV control through inhibition of NKG2A-expressing cells (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-01-05
    Description: The highly polymorphic human leukocyte antigen ( HLA ) locus encodes cell surface proteins that are critical for immunity. HLA-A expression levels vary in an allele-dependent manner, diversifying allele-specific effects beyond peptide-binding preference. Analysis of 9763 HIV-infected individuals from 21 cohorts shows that higher HLA-A levels confer poorer control of HIV. Elevated HLA-A expression provides enhanced levels of an HLA-A–derived signal peptide that specifically binds and determines expression levels of HLA-E, the ligand for the inhibitory NKG2A natural killer (NK) cell receptor. HLA-B haplotypes that favor NKG2A-mediated NK cell licensing (i.e., education) exacerbate the deleterious effect of high HLA-A on HIV control, consistent with NKG2A-mediated inhibition impairing NK cell clearance of HIV-infected targets. Therapeutic blockade of HLA-E:NKG2A interaction may yield benefit in HIV disease.
    Keywords: Genetics, Immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    MCL-1 is required throughout B-cell development and its loss sensitizes specific B-cell subsets to inhibition of BCL-2 or BCL-XL (2016)
    Springer Nature
    Details
    Publication Date: 2016-08-26
    Description: MCL-1 is required throughout B-cell development and its loss sensitizes specific B-cell subsets to inhibition of BCL-2 or BCL-XL Cell Death and Disease 7, e2345 (August 2016). doi:10.1038/cddis.2016.237 Authors: Ingela B Vikström, Anne Slomp, Emma M Carrington, Laura M Moesbergen, Catherine Chang, Gemma L Kelly, Stefan P Glaser, J H Marco Jansen, Jeanette H W Leusen, Andreas Strasser, David C S Huang, Andrew M Lew, Victor Peperzak & David M Tarlinton
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 6
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    mut-16 and other mutator class genes modulate 22G and 26G siRNA pathways in Caenorhabditis elegans [Genetics] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-01-26
    Description: Argonaute-associated siRNAs and Piwi-associated piRNAs have overlapping roles in silencing mobile genetic elements in animals. In Caenorhabditis elegans, mutator (mut) class genes mediate siRNA-guided repression of transposons as well as exogenous RNAi, but their roles in endogenous RNA silencing pathways are not well-understood. To characterize the endogenous small RNAs dependent on mut class genes, small RNA populations from a null allele of mut-16 as well as a regulatory mut-16(mg461) allele that disables only somatic RNAi were subjected to deep sequencing. Additionally, each of the mut class genes was tested for a requirement in 26G siRNA pathways. The results indicate that mut-16 is an essential factor in multiple endogenous germline and somatic siRNA pathways involving several distinct Argonautes and RNA-dependent RNA polymerases. The results also reveal essential roles for mut-2 and mut-7 in the ERGO-1 class 26G siRNA pathway and less critical roles for mut-8, mut-14, and mut-15. We show that transposons are hypersusceptible to mut-16–dependent silencing and identify a requirement for the siRNA machinery in piRNA biogenesis from Tc1 transposons. We also show that the soma-specific mut-16(mg461) mutant allele is present in multiple C. elegans laboratory strains.
    Keywords: Inaugural Articles
    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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  • 7
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    CCR5 promoter alleles and specific DNA binding factors (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bream, J H -- Young, H A -- Rice, N -- Martin, M P -- Smith, M W -- Carrington, M -- O'Brien, S J -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):223.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Experimental Immunology, National Cancer Institute-Frederick Cancer, Research and Development Center (NCI-FCRDC), Frederick, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15224670" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/immunology/mortality/*physiopathology ; *Alleles ; Binding Sites ; Cell Nucleus/metabolism ; DNA-Binding Proteins/*metabolism ; Disease Progression ; Electrophoretic Mobility Shift Assay ; Humans ; Nuclear Proteins/*metabolism ; Oligodeoxyribonucleotides/metabolism ; Polymorphism, Single Nucleotide ; *Promoter Regions, Genetic ; Receptors, CCR5/*genetics ; Survival Rate ; T-Lymphocytes ; Transcription Factors/metabolism
    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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  • 8
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    HLA and HIV-1: heterozygote advantage and B*35-Cw*04 disadvantage (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-12
    Description: A selective advantage against infectious disease associated with increased heterozygosity at the human major histocompatibility complex [human leukocyte antigen (HLA) class I and class II] is believed to play a major role in maintaining the extraordinary allelic diversity of these genes. Maximum HLA heterozygosity of class I loci (A, B, and C) delayed acquired immunodeficiency syndrome (AIDS) onset among patients infected with human immunodeficiency virus-type 1 (HIV-1), whereas individuals who were homozygous for one or more loci progressed rapidly to AIDS and death. The HLA class I alleles B*35 and Cw*04 were consistently associated with rapid development of AIDS-defining conditions in Caucasians. The extended survival of 28 to 40 percent of HIV-1-infected Caucasian patients who avoided AIDS for ten or more years can be attributed to their being fully heterozygous at HLA class I loci, to their lacking the AIDS-associated alleles B*35 and Cw*04, or to both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carrington, M -- Nelson, G W -- Martin, M P -- Kissner, T -- Vlahov, D -- Goedert, J J -- Kaslow, R -- Buchbinder, S -- Hoots, K -- O'Brien, S J -- N01-CO-56000/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 12;283(5408):1748-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Intramural Research Support Program, Science Applications International Corporation Frederick, National Cancer Institute (NCI), Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10073943" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/*immunology ; Adult ; Alleles ; Antigen Presentation ; Cohort Studies ; Disease Progression ; Ethnic Groups ; *Genes, MHC Class I ; Genetic Predisposition to Disease ; HIV Infections/genetics/*immunology ; HIV Long-Term Survivors/statistics & numerical data ; *Hiv-1 ; HLA Antigens/genetics ; HLA-B Antigens/*genetics ; HLA-C Antigens/*genetics ; Heterozygote ; Homozygote ; Humans ; Killer Cells, Natural/immunology ; Loss of Heterozygosity ; Proportional Hazards Models ; Risk
    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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  • 9
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    Genetic acceleration of AIDS progression by a promoter variant of CCR5 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-04
    Description: The CCR5 gene encodes a cell surface chemokine receptor molecule that serves as the principal coreceptor, with CD4, for macrophage-tropic (R5) strains of human immunodeficiency virus-type 1 (HIV-1). Genetic association analysis of five cohorts of people with acquired immunodeficiency syndrome (AIDS) revealed that infected individuals homozygous for a multisite haplotype of the CCR5 regulatory region containing the promoter allele, CCR5P1, progress to AIDS more rapidly than those with other CCR5 promoter genotypes, particularly in the early years after infection. Composite genetic epidemiologic analyses of genotypes bearing CCR5P1, CCR5-Delta32, CCR2-64I, and SDF1-3'A affirmed distinct regulatory influences for each gene on AIDS progression. An estimated 10 to 17 percent of patients who develop AIDS within 3.5 years of HIV-1 infection do so because they are homozygous for CCR5P1/P1, and 7 to 13 percent of all people carry this susceptible genotype. The cumulative and interactive influence of these AIDS restriction genes illustrates the multigenic nature of host factors limiting AIDS disease progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, M P -- Dean, M -- Smith, M W -- Winkler, C -- Gerrard, B -- Michael, N L -- Lee, B -- Doms, R W -- Margolick, J -- Buchbinder, S -- Goedert, J J -- O'Brien, T R -- Hilgartner, M W -- Vlahov, D -- O'Brien, S J -- Carrington, M -- N01-CO-56000/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1907-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Science Applications International Corporation (SAIC), National Cancer Institute, Frederick MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9836644" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/mortality/*physiopathology ; Alleles ; Chemokine CXCL12 ; Chemokines, CXC/genetics ; Cohort Studies ; Disease Progression ; Genes, Dominant ; Genes, Recessive ; Genetic Predisposition to Disease ; Genotype ; HIV Infections/genetics/physiopathology ; *Hiv-1 ; Haplotypes ; Heterozygote ; Homozygote ; Humans ; *Promoter Regions, Genetic ; Proportional Hazards Models ; Receptors, CCR2 ; Receptors, CCR5/*genetics ; *Receptors, Chemokine ; Receptors, Cytokine/*genetics ; Risk Factors ; Survival Rate
    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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  • 10
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    Genetic variation in IL28B and spontaneous clearance of hepatitis C virus (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-09-18
    Description: Hepatitis C virus (HCV) infection is the most common blood-borne infection in the United States, with estimates of 4 million HCV-infected individuals in the United States and 170 million worldwide. Most (70-80%) HCV infections persist and about 30% of individuals with persistent infection develop chronic liver disease, including cirrhosis and hepatocellular carcinoma. Epidemiological, viral and host factors have been associated with the differences in HCV clearance or persistence, and studies have demonstrated that a strong host immune response against HCV favours viral clearance. Thus, variation in genes involved in the immune response may contribute to the ability to clear the virus. In a recent genome-wide association study, a single nucleotide polymorphism (rs12979860) 3 kilobases upstream of the IL28B gene, which encodes the type III interferon IFN-3, was shown to associate strongly with more than a twofold difference in response to HCV drug treatment. To determine the potential effect of rs12979860 variation on outcome to HCV infection in a natural history setting, we genotyped this variant in HCV cohorts comprised of individuals who spontaneously cleared the virus (n = 388) or had persistent infection (n = 620). We show that the C/C genotype strongly enhances resolution of HCV infection among individuals of both European and African ancestry. To our knowledge, this is the strongest and most significant genetic effect associated with natural clearance of HCV, and these results implicate a primary role for IL28B in resolution of HCV infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3172006/" 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/PMC3172006/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, David L -- Thio, Chloe L -- Martin, Maureen P -- Qi, Ying -- Ge, Dongliang -- O'Huigin, Colm -- Kidd, Judith -- Kidd, Kenneth -- Khakoo, Salim I -- Alexander, Graeme -- Goedert, James J -- Kirk, Gregory D -- Donfield, Sharyne M -- Rosen, Hugo R -- Tobler, Leslie H -- Busch, Michael P -- McHutchison, John G -- Goldstein, David B -- Carrington, Mary -- HHSN261200800001E/CO/NCI NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- R01 DA004334/DA/NIDA NIH HHS/ -- R01DA004334/DA/NIDA NIH HHS/ -- R01DA013324/DA/NIDA NIH HHS/ -- R01DK60590/DK/NIDDK NIH HHS/ -- R01HD41224/HD/NICHD NIH HHS/ -- R01HL076902/HL/NHLBI NIH HHS/ -- R56 DA004334/DA/NIDA NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2009 Oct 8;461(7265):798-801. doi: 10.1038/nature08463.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins University, Division of Infectious Diseases, Baltimore, Maryland 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19759533" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Africa/ethnology ; Europe/ethnology ; Female ; Gene Frequency ; Genetic Variation/*genetics ; Genome-Wide Association Study ; Genotype ; Hepacivirus/drug effects/*immunology/physiology ; Hepatitis C/drug therapy/*genetics/*immunology/virology ; Humans ; Interleukins/*genetics/*immunology ; Male ; Polymorphism, Single Nucleotide/genetics
    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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