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  • 1
    Publication Date: 1999
    Description: Stable delivery of a therapeutic protein under pharmacologic control was achieved through in vivo somatic gene transfer. This system was based on the expression of two chimeric, human-derived proteins that were reconstituted by rapamycin into a transcription factor complex. A mixture of two adeno-associated virus vectors, one expressing the transcription factor chimeras and one containing erythropoietin (Epo) under the control of a promoter responsive to the transcription factor, was injected into skeletal muscle of immune-competent mice. Administration of rapamycin resulted in 200-fold induction of plasma Epo. Stable engraftment of this humanized system in immune-competent mice was achieved for 6 months with similar results for at least 3 months in a rhesus monkey.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, X -- Rivera, V M -- Zoltick, P -- Cerasoli, F Jr -- Schnell, M A -- Gao, G -- Hughes, J V -- Gilman, M -- Wilson, J M -- P01 AR/NS43648-03/AR/NIAMS NIH HHS/ -- P30 DK47757-05/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):88-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Human Gene Therapy, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytomegalovirus/genetics ; Dependovirus/genetics ; Erythropoietin/administration & dosage/blood/*genetics ; Female ; Gene Expression Regulation ; *Gene Transfer Techniques ; Genetic Therapy/*methods ; Genetic Vectors ; Hematocrit ; Injections, Intramuscular ; Macaca mulatta ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Muscle, Skeletal ; Promoter Regions, Genetic ; Recombinant Fusion Proteins ; Recombinant Proteins ; Sirolimus/*pharmacology ; Transcription Factors/*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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  • 2
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Virginia -- England -- Nature. 2010 Mar 18;464(7287):340-2. doi: 10.1038/464340a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237536" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antisocial Personality Disorder/physiopathology/psychology ; Child ; Female ; Forensic Sciences/ethics/*methods/trends ; Homicide/*legislation & jurisprudence/*psychology ; Humans ; Insanity Defense ; Magnetic Resonance Imaging/standards/*utilization ; Male ; *Neurosciences ; Positron-Emission Tomography/utilization ; Rape/legislation & jurisprudence/psychology ; Reproducibility of Results
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2010-01-15
    Description: The human Y chromosome began to evolve from an autosome hundreds of millions of years ago, acquiring a sex-determining function and undergoing a series of inversions that suppressed crossing over with the X chromosome. Little is known about the recent evolution of the Y chromosome because only the human Y chromosome has been fully sequenced. Prevailing theories hold that Y chromosomes evolve by gene loss, the pace of which slows over time, eventually leading to a paucity of genes, and stasis. These theories have been buttressed by partial sequence data from newly emergent plant and animal Y chromosomes, but they have not been tested in older, highly evolved Y chromosomes such as that of humans. Here we finished sequencing of the male-specific region of the Y chromosome (MSY) in our closest living relative, the chimpanzee, achieving levels of accuracy and completion previously reached for the human MSY. By comparing the MSYs of the two species we show that they differ radically in sequence structure and gene content, indicating rapid evolution during the past 6 million years. The chimpanzee MSY contains twice as many massive palindromes as the human MSY, yet it has lost large fractions of the MSY protein-coding genes and gene families present in the last common ancestor. We suggest that the extraordinary divergence of the chimpanzee and human MSYs was driven by four synergistic factors: the prominent role of the MSY in sperm production, 'genetic hitchhiking' effects in the absence of meiotic crossing over, frequent ectopic recombination within the MSY, and species differences in mating behaviour. Although genetic decay may be the principal dynamic in the evolution of newly emergent Y chromosomes, wholesale renovation is the paramount theme in the continuing evolution of chimpanzee, human and perhaps other older MSYs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653425/" 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/PMC3653425/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Jennifer F -- Skaletsky, Helen -- Pyntikova, Tatyana -- Graves, Tina A -- van Daalen, Saskia K M -- Minx, Patrick J -- Fulton, Robert S -- McGrath, Sean D -- Locke, Devin P -- Friedman, Cynthia -- Trask, Barbara J -- Mardis, Elaine R -- Warren, Wesley C -- Repping, Sjoerd -- Rozen, Steve -- Wilson, Richard K -- Page, David C -- R01 HG000257/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jan 28;463(7280):536-9. doi: 10.1038/nature08700. Epub 2010 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Whitehead Institute, and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20072128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Pair 21/genetics ; Chromosomes, Human, Y/*genetics ; DNA/chemistry/genetics ; Genes/*genetics ; Humans ; Male ; Molecular Sequence Data ; *Nucleic Acid Conformation ; Pan troglodytes/*genetics ; Sequence Homology, Nucleic Acid ; Y Chromosome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2007-04-28
    Description: New strategies for prevention and treatment of type 2 diabetes (T2D) require improved insight into disease etiology. We analyzed 386,731 common single-nucleotide polymorphisms (SNPs) in 1464 patients with T2D and 1467 matched controls, each characterized for measures of glucose metabolism, lipids, obesity, and blood pressure. With collaborators (FUSION and WTCCC/UKT2D), we identified and confirmed three loci associated with T2D-in a noncoding region near CDKN2A and CDKN2B, in an intron of IGF2BP2, and an intron of CDKAL1-and replicated associations near HHEX and in SLC30A8 found by a recent whole-genome association study. We identified and confirmed association of a SNP in an intron of glucokinase regulatory protein (GCKR) with serum triglycerides. The discovery of associated variants in unsuspected genes and outside coding regions illustrates the ability of genome-wide association studies to provide potentially important clues to the pathogenesis of common diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diabetes Genetics Initiative of Broad Institute of Harvard and MIT, Lund University, and Novartis Institutes of BioMedical Research -- Saxena, Richa -- Voight, Benjamin F -- Lyssenko, Valeriya -- Burtt, Noel P -- de Bakker, Paul I W -- Chen, Hong -- Roix, Jeffrey J -- Kathiresan, Sekar -- Hirschhorn, Joel N -- Daly, Mark J -- Hughes, Thomas E -- Groop, Leif -- Altshuler, David -- Almgren, Peter -- Florez, Jose C -- Meyer, Joanne -- Ardlie, Kristin -- Bengtsson Bostrom, Kristina -- Isomaa, Bo -- Lettre, Guillaume -- Lindblad, Ulf -- Lyon, Helen N -- Melander, Olle -- Newton-Cheh, Christopher -- Nilsson, Peter -- Orho-Melander, Marju -- Rastam, Lennart -- Speliotes, Elizabeth K -- Taskinen, Marja-Riitta -- Tuomi, Tiinamaija -- Guiducci, Candace -- Berglund, Anna -- Carlson, Joyce -- Gianniny, Lauren -- Hackett, Rachel -- Hall, Liselotte -- Holmkvist, Johan -- Laurila, Esa -- Sjogren, Marketa -- Sterner, Maria -- Surti, Aarti -- Svensson, Margareta -- Svensson, Malin -- Tewhey, Ryan -- Blumenstiel, Brendan -- Parkin, Melissa -- Defelice, Matthew -- Barry, Rachel -- Brodeur, Wendy -- Camarata, Jody -- Chia, Nancy -- Fava, Mary -- Gibbons, John -- Handsaker, Bob -- Healy, Claire -- Nguyen, Kieu -- Gates, Casey -- Sougnez, Carrie -- Gage, Diane -- Nizzari, Marcia -- Gabriel, Stacey B -- Chirn, Gung-Wei -- Ma, Qicheng -- Parikh, Hemang -- Richardson, Delwood -- Ricke, Darrell -- Purcell, Shaun -- F32 DK079466/DK/NIDDK NIH HHS/ -- F32 DK079466-01/DK/NIDDK NIH HHS/ -- K23 DK067288/DK/NIDDK NIH HHS/ -- K23 DK080145/DK/NIDDK NIH HHS/ -- K23 DK080145-01/DK/NIDDK NIH HHS/ -- K23 DK65978-04/DK/NIDDK NIH HHS/ -- K23-HL083102/HL/NHLBI NIH HHS/ -- U01 HG004171/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1331-6. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Harvard and Massachusetts Institute of Technology (MIT), Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463246" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics ; Aged ; Alleles ; Blood Glucose/analysis ; Case-Control Studies ; Chromosome Mapping ; Chromosomes, Human, Pair 9/genetics ; Diabetes Mellitus, Type 2/*genetics ; Female ; Genetic Markers ; *Genetic Predisposition to Disease ; *Genome, Human ; Genotype ; Haplotypes ; Humans ; Insulin Resistance/genetics ; Insulin-Like Growth Factor Binding Proteins/genetics ; Introns ; Male ; Meta-Analysis as Topic ; Middle Aged ; *Polymorphism, Single Nucleotide ; Quantitative Trait, Heritable ; Triglycerides/*blood
    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
    Publication Date: 2008-05-31
    Description: Close relatedness has long been considered crucial to the evolution of eusociality. However, it has recently been suggested that close relatedness may be a consequence, rather than a cause, of eusociality. We tested this idea with a comparative analysis of female mating frequencies in 267 species of eusocial bees, wasps, and ants. We found that mating with a single male, which maximizes relatedness, is ancestral for all eight independent eusocial lineages that we investigated. Mating with multiple males is always derived. Furthermore, we found that high polyandry (〉2 effective mates) occurs only in lineages whose workers have lost reproductive totipotency. These results provide the first evidence that monogamy was critical in the evolution of eusociality, strongly supporting the prediction of inclusive fitness theory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, William O H -- Oldroyd, Benjamin P -- Beekman, Madeleine -- Ratnieks, Francis L W -- New York, N.Y. -- Science. 2008 May 30;320(5880):1213-6. doi: 10.1126/science.1156108.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Integrative and Comparative Biology, University of Leeds, Leeds, LS2 9JT, UK. w.o.h.hughes@leeds.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18511689" target="_blank"〉PubMed〈/a〉
    Keywords: Altruism ; Animals ; Ants ; Bees ; *Biological Evolution ; Female ; Male ; Phylogeny ; *Sexual Behavior, Animal ; *Social Behavior ; Sociobiology ; Wasps
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2012-03-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Katherine J -- Kennedy, Brian K -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1578-9. doi: 10.1126/science.1221365.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Buck Institute for Research on Aging, Novato, CA 94945, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; *Insulin Resistance ; *Longevity ; Male ; Sirolimus/*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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  • 7
    Publication Date: 2012-10-16
    Description: The rhg1-b allele of soybean is widely used for resistance against soybean cyst nematode (SCN), the most economically damaging pathogen of soybeans in the United States. Gene silencing showed that genes in a 31-kilobase segment at rhg1-b, encoding an amino acid transporter, an alpha-SNAP protein, and a WI12 (wound-inducible domain) protein, each contribute to resistance. There is one copy of the 31-kilobase segment per haploid genome in susceptible varieties, but 10 tandem copies are present in an rhg1-b haplotype. Overexpression of the individual genes in roots was ineffective, but overexpression of the genes together conferred enhanced SCN resistance. Hence, SCN resistance mediated by the soybean quantitative trait locus Rhg1 is conferred by copy number variation that increases the expression of a set of dissimilar genes in a repeated multigene segment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, David E -- Lee, Tong Geon -- Guo, Xiaoli -- Melito, Sara -- Wang, Kai -- Bayless, Adam M -- Wang, Jianping -- Hughes, Teresa J -- Willis, David K -- Clemente, Thomas E -- Diers, Brian W -- Jiang, Jiming -- Hudson, Matthew E -- Bent, Andrew F -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1206-9. doi: 10.1126/science.1228746. Epub 2012 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23065905" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; *Gene Dosage ; Gene Expression Regulation, Plant ; *Genetic Loci ; Genetic Variation ; Haplotypes ; Male ; Molecular Sequence Data ; Plant Diseases/*genetics/*parasitology ; Plant Proteins/*genetics ; Plant Roots/genetics/parasitology ; Protein Structure, Tertiary/genetics ; Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins/genetics ; Soybeans/*genetics/*parasitology ; *Tylenchoidea
    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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  • 8
    Publication Date: 2013-05-25
    Description: CD8(+) T cell responses focus on a small fraction of pathogen- or vaccine-encoded peptides, and for some pathogens, these restricted recognition hierarchies limit the effectiveness of antipathogen immunity. We found that simian immunodeficiency virus (SIV) protein-expressing rhesus cytomegalovirus (RhCMV) vectors elicit SIV-specific CD8(+) T cells that recognize unusual, diverse, and highly promiscuous epitopes, including dominant responses to epitopes restricted by class II major histocompatibility complex (MHC) molecules. Induction of canonical SIV epitope-specific CD8(+) T cell responses is suppressed by the RhCMV-encoded Rh189 gene (corresponding to human CMV US11), and the promiscuous MHC class I- and class II-restricted CD8(+) T cell responses occur only in the absence of the Rh157.5, Rh157.4, and Rh157.6 (human CMV UL128, UL130, and UL131) genes. Thus, CMV vectors can be genetically programmed to achieve distinct patterns of CD8(+) T cell epitope recognition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3816976/" 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/PMC3816976/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, Scott G -- Sacha, Jonah B -- Hughes, Colette M -- Ford, Julia C -- Burwitz, Benjamin J -- Scholz, Isabel -- Gilbride, Roxanne M -- Lewis, Matthew S -- Gilliam, Awbrey N -- Ventura, Abigail B -- Malouli, Daniel -- Xu, Guangwu -- Richards, Rebecca -- Whizin, Nathan -- Reed, Jason S -- Hammond, Katherine B -- Fischer, Miranda -- Turner, John M -- Legasse, Alfred W -- Axthelm, Michael K -- Edlefsen, Paul T -- Nelson, Jay A -- Lifson, Jeffrey D -- Fruh, Klaus -- Picker, Louis J -- P01 AI094417/AI/NIAID NIH HHS/ -- P51 OD 011092/OD/NIH HHS/ -- R01 AI059457/AI/NIAID NIH HHS/ -- R01 AI060392/AI/NIAID NIH HHS/ -- U24 OD010850/OD/NIH HHS/ -- New York, N.Y. -- Science. 2013 May 24;340(6135):1237874. doi: 10.1126/science.1237874.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine and Gene Therapy Institute and Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, OR 97006, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704576" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Cytokines/immunology ; Cytomegalovirus/genetics/*immunology ; Epitopes, T-Lymphocyte/*immunology ; Female ; Genetic Vectors/genetics/*immunology ; Histocompatibility Antigens Class II/immunology ; Humans ; Macaca mulatta ; Male ; Membrane Glycoproteins/genetics ; SAIDS Vaccines/administration & dosage/*immunology ; Viral Envelope Proteins/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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  • 9
    Publication Date: 2011-05-13
    Description: The acquired immunodeficiency syndrome (AIDS)-causing lentiviruses human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) effectively evade host immunity and, once established, infections with these viruses are only rarely controlled by immunological mechanisms. However, the initial establishment of infection in the first few days after mucosal exposure, before viral dissemination and massive replication, may be more vulnerable to immune control. Here we report that SIV vaccines that include rhesus cytomegalovirus (RhCMV) vectors establish indefinitely persistent, high-frequency, SIV-specific effector memory T-cell (T(EM)) responses at potential sites of SIV replication in rhesus macaques and stringently control highly pathogenic SIV(MAC239) infection early after mucosal challenge. Thirteen of twenty-four rhesus macaques receiving either RhCMV vectors alone or RhCMV vectors followed by adenovirus 5 (Ad5) vectors (versus 0 of 9 DNA/Ad5-vaccinated rhesus macaques) manifested early complete control of SIV (undetectable plasma virus), and in twelve of these thirteen animals we observed long-term (〉/=1 year) protection. This was characterized by: occasional blips of plasma viraemia that ultimately waned; predominantly undetectable cell-associated viral load in blood and lymph node mononuclear cells; no depletion of effector-site CD4(+) memory T cells; no induction or boosting of SIV Env-specific antibodies; and induction and then loss of T-cell responses to an SIV protein (Vif) not included in the RhCMV vectors. Protection correlated with the magnitude of the peak SIV-specific CD8(+) T-cell responses in the vaccine phase, and occurred without anamnestic T-cell responses. Remarkably, long-term RhCMV vector-associated SIV control was insensitive to either CD8(+) or CD4(+) lymphocyte depletion and, at necropsy, cell-associated SIV was only occasionally measurable at the limit of detection with ultrasensitive assays, observations that indicate the possibility of eventual viral clearance. Thus, persistent vectors such as CMV and their associated T(EM) responses might significantly contribute to an efficacious HIV/AIDS vaccine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102768/" 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/PMC3102768/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, Scott G -- Ford, Julia C -- Lewis, Matthew S -- Ventura, Abigail B -- Hughes, Colette M -- Coyne-Johnson, Lia -- Whizin, Nathan -- Oswald, Kelli -- Shoemaker, Rebecca -- Swanson, Tonya -- Legasse, Alfred W -- Chiuchiolo, Maria J -- Parks, Christopher L -- Axthelm, Michael K -- Nelson, Jay A -- Jarvis, Michael A -- Piatak, Michael Jr -- Lifson, Jeffrey D -- Picker, Louis J -- HHSN261200800001E/PHS HHS/ -- HHSN272200900037C/PHS HHS/ -- P51 RR00163/RR/NCRR NIH HHS/ -- R01 AI060392/AI/NIAID NIH HHS/ -- R01 AI060392-05/AI/NIAID NIH HHS/ -- R24 RR016001/RR/NCRR NIH HHS/ -- R56 AI060392/AI/NIAID NIH HHS/ -- R56 AI060392-06/AI/NIAID NIH HHS/ -- U24 OD010850/OD/NIH HHS/ -- England -- Nature. 2011 May 26;473(7348):523-7. doi: 10.1038/nature10003. Epub 2011 May 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine and Gene Therapy Institute, Department of Molecular Microbiology, Oregon Health & Science University, Beaverton, Oregon 97006, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21562493" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/immunology ; Animals ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cytomegalovirus/genetics ; DNA, Viral/analysis ; Genetic Vectors/genetics ; Immunity, Mucosal/immunology ; Immunologic Memory/*immunology ; Macaca mulatta/blood/immunology/virology ; Male ; RNA, Viral/analysis ; SAIDS Vaccines/genetics/*immunology ; Simian Acquired Immunodeficiency Syndrome/blood/*immunology/*prevention & ; control/virology ; Simian Immunodeficiency Virus/growth & development/*immunology/isolation & ; purification/*pathogenicity ; T-Lymphocytes/*immunology ; Time Factors ; Vaccines, DNA/genetics/immunology ; Viral Load ; Virus Replication
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2012-03-01
    Description: The human X and Y chromosomes evolved from an ordinary pair of autosomes during the past 200-300 million years. The human MSY (male-specific region of Y chromosome) retains only three percent of the ancestral autosomes' genes owing to genetic decay. This evolutionary decay was driven by a series of five 'stratification' events. Each event suppressed X-Y crossing over within a chromosome segment or 'stratum', incorporated that segment into the MSY and subjected its genes to the erosive forces that attend the absence of crossing over. The last of these events occurred 30 million years ago, 5 million years before the human and Old World monkey lineages diverged. Although speculation abounds regarding ongoing decay and looming extinction of the human Y chromosome, remarkably little is known about how many MSY genes were lost in the human lineage in the 25 million years that have followed its separation from the Old World monkey lineage. To investigate this question, we sequenced the MSY of the rhesus macaque, an Old World monkey, and compared it to the human MSY. We discovered that during the last 25 million years MSY gene loss in the human lineage was limited to the youngest stratum (stratum 5), which comprises three percent of the human MSY. In the older strata, which collectively comprise the bulk of the human MSY, gene loss evidently ceased more than 25 million years ago. Likewise, the rhesus MSY has not lost any older genes (from strata 1-4) during the past 25 million years, despite its major structural differences to the human MSY. The rhesus MSY is simpler, with few amplified gene families or palindromes that might enable intrachromosomal recombination and repair. We present an empirical reconstruction of human MSY evolution in which each stratum transitioned from rapid, exponential loss of ancestral genes to strict conservation through purifying selection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292678/" 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/PMC3292678/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, Jennifer F -- Skaletsky, Helen -- Brown, Laura G -- Pyntikova, Tatyana -- Graves, Tina -- Fulton, Robert S -- Dugan, Shannon -- Ding, Yan -- Buhay, Christian J -- Kremitzki, Colin -- Wang, Qiaoyan -- Shen, Hua -- Holder, Michael -- Villasana, Donna -- Nazareth, Lynne V -- Cree, Andrew -- Courtney, Laura -- Veizer, Joelle -- Kotkiewicz, Holland -- Cho, Ting-Jan -- Koutseva, Natalia -- Rozen, Steve -- Muzny, Donna M -- Warren, Wesley C -- Gibbs, Richard A -- Wilson, Richard K -- Page, David C -- R01 HG000257/HG/NHGRI NIH HHS/ -- R01 HG000257-17/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 22;483(7387):82-6. doi: 10.1038/nature10843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA. jhughes@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22367542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Y/*genetics ; Conserved Sequence/*genetics ; Crossing Over, Genetic/genetics ; *Evolution, Molecular ; Gene Amplification/genetics ; *Gene Deletion ; Humans ; In Situ Hybridization, Fluorescence ; Macaca mulatta/*genetics ; Male ; Models, Genetic ; Molecular Sequence Data ; Pan troglodytes/genetics ; Radiation Hybrid Mapping ; Selection, Genetic/genetics ; Time Factors ; Y Chromosome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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