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  • 1
    Publication Date: 2006-11-18
    Description: Our knowledge of Neanderthals is based on a limited number of remains and artifacts from which we must make inferences about their biology, behavior, and relationship to ourselves. Here, we describe the characterization of these extinct hominids from a new perspective, based on the development of a Neanderthal metagenomic library and its high-throughput sequencing and analysis. Several lines of evidence indicate that the 65,250 base pairs of hominid sequence so far identified in the library are of Neanderthal origin, the strongest being the ascertainment of sequence identities between Neanderthal and chimpanzee at sites where the human genomic sequence is different. These results enabled us to calculate the human-Neanderthal divergence time based on multiple randomly distributed autosomal loci. Our analyses suggest that on average the Neanderthal genomic sequence we obtained and the reference human genome sequence share a most recent common ancestor approximately 706,000 years ago, and that the human and Neanderthal ancestral populations split approximately 370,000 years ago, before the emergence of anatomically modern humans. Our finding that the Neanderthal and human genomes are at least 99.5% identical led us to develop and successfully implement a targeted method for recovering specific ancient DNA sequences from metagenomic libraries. This initial analysis of the Neanderthal genome advances our understanding of the evolutionary relationship of Homo sapiens and Homo neanderthalensis and signifies the dawn of Neanderthal genomics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583069/" 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/PMC2583069/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noonan, James P -- Coop, Graham -- Kudaravalli, Sridhar -- Smith, Doug -- Krause, Johannes -- Alessi, Joe -- Chen, Feng -- Platt, Darren -- Paabo, Svante -- Pritchard, Jonathan K -- Rubin, Edward M -- 1-F32-GM074367/GM/NIGMS NIH HHS/ -- HL066681/HL/NHLBI NIH HHS/ -- R01 HG002772/HG/NHGRI NIH HHS/ -- R01 HG002772-01/HG/NHGRI NIH HHS/ -- R01 HG002772-1/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1113-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Energy Joint Genome Institute, 2800 Mitchell Drive, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones ; Cell Nucleus ; DNA/*genetics/isolation & purification ; DNA, Mitochondrial ; *Fossils ; Gene Pool ; Genome ; Genome, Human ; Genomic Library ; History, Ancient ; Hominidae/*genetics ; Humans ; Male ; Molecular Sequence Data ; Pan troglodytes/genetics ; Polymerase Chain Reaction ; Sequence Alignment ; *Sequence Analysis, DNA/methods ; Time
    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
    Publication Date: 2008-02-02
    Description: Recombination plays a crucial role in meiosis, ensuring the proper segregation of chromosomes. Recent linkage disequilibrium (LD) and sperm-typing studies suggest that recombination rates vary tremendously across the human genome, with most events occurring in narrow "hotspots." To examine variation in fine-scale recombination patterns among individuals, we used dense, genome-wide single-nucleotide polymorphism data collected in nuclear families to localize crossovers with high spatial resolution. This analysis revealed that overall recombination hotspot usage is similar in males and females, with individual hotspots often active in both sexes. Across the genome, roughly 60% of crossovers occurred in hotspots inferred from LD studies. Notably, however, we found extensive and heritable variation among both males and females in the proportion of crossovers occurring in these hotspots.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coop, Graham -- Wen, Xiaoquan -- Ober, Carole -- Pritchard, Jonathan K -- Przeworski, Molly -- GM83098/GM/NIGMS NIH HHS/ -- HD21244/HD/NICHD NIH HHS/ -- HG002772/HG/NHGRI NIH HHS/ -- HL56399/HL/NHLBI NIH HHS/ -- HL56533/HL/NHLBI NIH HHS/ -- R01 HG002772/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 7;319(5868):1395-8. doi: 10.1126/science.1151851. Epub 2008 Jan 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Chicago, 920 East 58th Street, Cummings Life Science Center, Chicago, IL 60637, USA. gcoop@uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239090" target="_blank"〉PubMed〈/a〉
    Keywords: *Crossing Over, Genetic ; Female ; Genetic Variation ; *Genome, Human ; Genotype ; Haplotypes ; Humans ; Linkage Disequilibrium ; Male ; Maternal Age ; Meiosis ; Paternal Age ; Pedigree ; Polymorphism, Single Nucleotide ; *Recombination, Genetic ; Sex Characteristics ; Transcription Initiation Site
    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
    Publication Date: 2012-02-22
    Description: Genome-sequencing studies indicate that all humans carry many genetic variants predicted to cause loss of function (LoF) of protein-coding genes, suggesting unexpected redundancy in the human genome. Here we apply stringent filters to 2951 putative LoF variants obtained from 185 human genomes to determine their true prevalence and properties. We estimate that human genomes typically contain ~100 genuine LoF variants with ~20 genes completely inactivated. We identify rare and likely deleterious LoF alleles, including 26 known and 21 predicted severe disease-causing variants, as well as common LoF variants in nonessential genes. We describe functional and evolutionary differences between LoF-tolerant and recessive disease genes and a method for using these differences to prioritize candidate genes found in clinical sequencing studies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299548/" 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/PMC3299548/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacArthur, Daniel G -- Balasubramanian, Suganthi -- Frankish, Adam -- Huang, Ni -- Morris, James -- Walter, Klaudia -- Jostins, Luke -- Habegger, Lukas -- Pickrell, Joseph K -- Montgomery, Stephen B -- Albers, Cornelis A -- Zhang, Zhengdong D -- Conrad, Donald F -- Lunter, Gerton -- Zheng, Hancheng -- Ayub, Qasim -- DePristo, Mark A -- Banks, Eric -- Hu, Min -- Handsaker, Robert E -- Rosenfeld, Jeffrey A -- Fromer, Menachem -- Jin, Mike -- Mu, Xinmeng Jasmine -- Khurana, Ekta -- Ye, Kai -- Kay, Mike -- Saunders, Gary Ian -- Suner, Marie-Marthe -- Hunt, Toby -- Barnes, If H A -- Amid, Clara -- Carvalho-Silva, Denise R -- Bignell, Alexandra H -- Snow, Catherine -- Yngvadottir, Bryndis -- Bumpstead, Suzannah -- Cooper, David N -- Xue, Yali -- Romero, Irene Gallego -- 1000 Genomes Project Consortium -- Wang, Jun -- Li, Yingrui -- Gibbs, Richard A -- McCarroll, Steven A -- Dermitzakis, Emmanouil T -- Pritchard, Jonathan K -- Barrett, Jeffrey C -- Harrow, Jennifer -- Hurles, Matthew E -- Gerstein, Mark B -- Tyler-Smith, Chris -- 085532/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- BB/I02593X/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- RG/09/012/28096/British Heart Foundation/United Kingdom -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Feb 17;335(6070):823-8. doi: 10.1126/science.1215040.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, UK. macarthur@atgu.mgh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22344438" target="_blank"〉PubMed〈/a〉
    Keywords: Disease/genetics ; Gene Expression ; Gene Frequency ; *Genetic Variation ; *Genome, Human ; Humans ; Phenotype ; Polymorphism, Single Nucleotide ; Proteins/*genetics ; Selection, Genetic
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    Electronic ISSN: 1095-9203
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  • 4
    Publication Date: 2003-03-08
    Description: Helicobacter pylori, a chronic gastric pathogen of human beings, can be divided into seven populations and subpopulations with distinct geographical distributions. These modern populations derive their gene pools from ancestral populations that arose in Africa, Central Asia, and East Asia. Subsequent spread can be attributed to human migratory fluxes such as the prehistoric colonization of Polynesia and the Americas, the neolithic introduction of farming to Europe, the Bantu expansion within Africa, and the slave trade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Falush, Daniel -- Wirth, Thierry -- Linz, Bodo -- Pritchard, Jonathan K -- Stephens, Matthew -- Kidd, Mark -- Blaser, Martin J -- Graham, David Y -- Vacher, Sylvie -- Perez-Perez, Guillermo I -- Yamaoka, Yoshio -- Megraud, Francis -- Otto, Kristina -- Reichard, Ulrike -- Katzowitsch, Elena -- Wang, Xiaoyan -- Achtman, Mark -- Suerbaum, Sebastian -- R02GM63270/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Max-Planck Institut fur Infektionsbiologie, 10117 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624269" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Agriculture ; Americas ; Asia ; Bacterial Proteins/genetics ; Bayes Theorem ; Continental Population Groups ; *Emigration and Immigration ; Ethnic Groups ; Europe ; Genes, Bacterial ; Genetic Variation ; *Genetics, Population ; Geography ; Helicobacter Infections/*microbiology/transmission ; Helicobacter pylori/classification/*genetics/isolation & purification ; Humans ; Indians, North American ; Language ; *Polymorphism, Genetic ; Polynesia ; Recombination, Genetic ; Social Problems ; Software
    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: 2002-12-21
    Description: We studied human population structure using genotypes at 377 autosomal microsatellite loci in 1056 individuals from 52 populations. Within-population differences among individuals account for 93 to 95% of genetic variation; differences among major groups constitute only 3 to 5%. Nevertheless, without using prior information about the origins of individuals, we identified six main genetic clusters, five of which correspond to major geographic regions, and subclusters that often correspond to individual populations. General agreement of genetic and predefined populations suggests that self-reported ancestry can facilitate assessments of epidemiological risks but does not obviate the need to use genetic information in genetic association studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, Noah A -- Pritchard, Jonathan K -- Weber, James L -- Cann, Howard M -- Kidd, Kenneth K -- Zhivotovsky, Lev A -- Feldman, Marcus W -- GM28428/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Dec 20;298(5602):2381-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Computational Biology, 1042 West 36th Place DRB 289, University of Southern California, Los Angeles, CA 90089, USA. noahr@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12493913" target="_blank"〉PubMed〈/a〉
    Keywords: Africa South of the Sahara ; Algorithms ; Alleles ; Americas ; Analysis of Variance ; Asia ; Cluster Analysis ; Europe ; Gene Frequency ; Genetic Drift ; Genetic Predisposition to Disease ; *Genetic Variation ; *Genetics, Medical ; *Genetics, Population ; Genotype ; Geography ; Heterozygote ; Humans ; Language ; Microsatellite Repeats ; Middle East ; Pacific Islands ; Probability ; Risk Factors
    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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  • 6
    Publication Date: 2013-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birney, Ewan -- Pritchard, Jonathan K -- England -- Nature. 2014 Jan 2;505(7481):32-4. doi: 10.1038/nature12847. Epub 2013 Dec 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Cambridge CB10 1SD, UK. ; Departments of Genetics and Biology and the Howard Hughes Medical Institute, Stanford University, Stanford, California 94305-5120, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24352230" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; *Fossils ; Genome/*genetics ; Humans ; Neanderthals/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2012-09-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ecker, Joseph R -- Bickmore, Wendy A -- Barroso, Ines -- Pritchard, Jonathan K -- Gilad, Yoav -- Segal, Eran -- England -- Nature. 2012 Sep 6;489(7414):52-5. doi: 10.1038/489052a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and the Salk Institute for Biological Studies, La Jolla, California 92037, USA. ecker@salk.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22955614" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatin/genetics/metabolism ; DNA/*genetics ; DNA Methylation ; Deoxyribonuclease I/metabolism ; *Encyclopedias as Topic ; Evolution, Molecular ; Gene Expression Regulation/genetics ; Gene Regulatory Networks ; Genome, Human/*genetics ; *Genomics/trends ; Humans ; Interdisciplinary Communication ; *Molecular Sequence Annotation ; RNA, Untranslated/genetics ; Regulatory Sequences, Nucleic Acid/*genetics ; Sequence Analysis ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2010-03-12
    Description: Understanding the genetic mechanisms underlying natural variation in gene expression is a central goal of both medical and evolutionary genetics, and studies of expression quantitative trait loci (eQTLs) have become an important tool for achieving this goal. Although all eQTL studies so far have assayed messenger RNA levels using expression microarrays, recent advances in RNA sequencing enable the analysis of transcript variation at unprecedented resolution. We sequenced RNA from 69 lymphoblastoid cell lines derived from unrelated Nigerian individuals that have been extensively genotyped by the International HapMap Project. By pooling data from all individuals, we generated a map of the transcriptional landscape of these cells, identifying extensive use of unannotated untranslated regions and more than 100 new putative protein-coding exons. Using the genotypes from the HapMap project, we identified more than a thousand genes at which genetic variation influences overall expression levels or splicing. We demonstrate that eQTLs near genes generally act by a mechanism involving allele-specific expression, and that variation that influences the inclusion of an exon is enriched within and near the consensus splice sites. Our results illustrate the power of high-throughput sequencing for the joint analysis of variation in transcription, splicing and allele-specific expression across individuals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089435/" 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/PMC3089435/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pickrell, Joseph K -- Marioni, John C -- Pai, Athma A -- Degner, Jacob F -- Engelhardt, Barbara E -- Nkadori, Everlyne -- Veyrieras, Jean-Baptiste -- Stephens, Matthew -- Gilad, Yoav -- Pritchard, Jonathan K -- GM077959/GM/NIGMS NIH HHS/ -- MH084703-01/MH/NIMH NIH HHS/ -- R01 GM077959/GM/NIGMS NIH HHS/ -- R01 GM077959-05/GM/NIGMS NIH HHS/ -- R01 MH084703/MH/NIMH NIH HHS/ -- R01 MH084703-02/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Apr 1;464(7289):768-72. doi: 10.1038/nature08872. Epub 2010 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, The University of Chicago, Chicago 60637, USA. pickrell@uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220758" target="_blank"〉PubMed〈/a〉
    Keywords: African Continental Ancestry Group/genetics ; Alleles ; Consensus Sequence/genetics ; DNA, Complementary/genetics ; Exons/genetics ; *Gene Expression Profiling ; Gene Expression Regulation/*genetics ; Genetic Variation/*genetics ; Humans ; Nigeria ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics ; RNA Splice Sites/genetics ; RNA, Messenger/*analysis/*genetics ; Sequence Analysis, RNA ; Transcription, Genetic/*genetics
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  • 9
    Publication Date: 2012-02-07
    Description: The mapping of expression quantitative trait loci (eQTLs) has emerged as an important tool for linking genetic variation to changes in gene regulation. However, it remains difficult to identify the causal variants underlying eQTLs, and little is known about the regulatory mechanisms by which they act. Here we show that genetic variants that modify chromatin accessibility and transcription factor binding are a major mechanism through which genetic variation leads to gene expression differences among humans. We used DNase I sequencing to measure chromatin accessibility in 70 Yoruba lymphoblastoid cell lines, for which genome-wide genotypes and estimates of gene expression levels are also available. We obtained a total of 2.7 billion uniquely mapped DNase I-sequencing (DNase-seq) reads, which allowed us to produce genome-wide maps of chromatin accessibility for each individual. We identified 8,902 locations at which the DNase-seq read depth correlated significantly with genotype at a nearby single nucleotide polymorphism or insertion/deletion (false discovery rate = 10%). We call such variants 'DNase I sensitivity quantitative trait loci' (dsQTLs). We found that dsQTLs are strongly enriched within inferred transcription factor binding sites and are frequently associated with allele-specific changes in transcription factor binding. A substantial fraction (16%) of dsQTLs are also associated with variation in the expression levels of nearby genes (that is, these loci are also classified as eQTLs). Conversely, we estimate that as many as 55% of eQTL single nucleotide polymorphisms are also dsQTLs. Our observations indicate that dsQTLs are highly abundant in the human genome and are likely to be important contributors to phenotypic variation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501342/" 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/PMC3501342/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Degner, Jacob F -- Pai, Athma A -- Pique-Regi, Roger -- Veyrieras, Jean-Baptiste -- Gaffney, Daniel J -- Pickrell, Joseph K -- De Leon, Sherryl -- Michelini, Katelyn -- Lewellen, Noah -- Crawford, Gregory E -- Stephens, Matthew -- Gilad, Yoav -- Pritchard, Jonathan K -- HG006123/HG/NHGRI NIH HHS/ -- MH084703/MH/NIMH NIH HHS/ -- MH090951/MH/NIMH NIH HHS/ -- R01 HG006123/HG/NHGRI NIH HHS/ -- R01 HG006123-01/HG/NHGRI NIH HHS/ -- R01 HG006123-02/HG/NHGRI NIH HHS/ -- R01 MH090951/MH/NIMH NIH HHS/ -- R01 MH090951-01/MH/NIMH NIH HHS/ -- R01 MH090951-02/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 5;482(7385):390-4. doi: 10.1038/nature10808.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Chicago, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22307276" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatin/genetics/metabolism ; *DNA Footprinting ; Deoxyribonuclease I/*metabolism ; Gene Expression Profiling ; Gene Expression Regulation/*genetics ; Genetic Variation/*genetics ; Genome, Human/genetics ; Humans ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/*genetics ; Sequence Analysis, DNA ; Transcription Factors/metabolism
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1996-11-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pritchard, J K -- Feldman, M W -- New York, N.Y. -- Science. 1996 Nov 29;274(5292):1548a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17816997" target="_blank"〉PubMed〈/a〉
    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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