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  • 1
    Publication Date: 2002-03-30
    Description: To begin to understand the genetic architecture of natural variation in gene expression, we carried out genetic linkage analysis of genomewide expression patterns in a cross between a laboratory strain and a wild strain of Saccharomyces cerevisiae. Over 1500 genes were differentially expressed between the parent strains. Expression levels of 570 genes were linked to one or more different loci, with most expression levels showing complex inheritance patterns. The loci detected by linkage fell largely into two categories: cis-acting modulators of single genes and trans-acting modulators of many genes. We found eight such trans-acting loci, each affecting the expression of a group of 7 to 94 genes of related function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brem, Rachel B -- Yvert, Gael -- Clinton, Rebecca -- Kruglyak, Leonid -- GM64268/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):752-5. Epub 2002 Mar 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center (FHCRC), 1100 Fairview Avenue North, D4-100, Seattle, WA 98109, USA and Howard Hughes Medical Institute.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11923494" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; Crosses, Genetic ; *DNA-Binding Proteins ; Fungal Proteins/genetics/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Fungal ; Genes, Fungal ; Genetic Linkage ; Genetic Markers ; Genome, Fungal ; Genotype ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Genetic ; RNA, Fungal/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Regulatory Sequences, Nucleic Acid ; Saccharomyces cerevisiae/*genetics/growth & development/physiology ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/metabolism ; *Transcription, Genetic
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  • 2
    Publication Date: 1998-06-06
    Description: Single-nucleotide polymorphisms (SNPs) are the most frequent type of variation in the human genome, and they provide powerful tools for a variety of medical genetic studies. In a large-scale survey for SNPs, 2.3 megabases of human genomic DNA was examined by a combination of gel-based sequencing and high-density variation-detection DNA chips. A total of 3241 candidate SNPs were identified. A genetic map was constructed showing the location of 2227 of these SNPs. Prototype genotyping chips were developed that allow simultaneous genotyping of 500 SNPs. The results provide a characterization of human diversity at the nucleotide level and demonstrate the feasibility of large-scale identification of human SNPs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, D G -- Fan, J B -- Siao, C J -- Berno, A -- Young, P -- Sapolsky, R -- Ghandour, G -- Perkins, N -- Winchester, E -- Spencer, J -- Kruglyak, L -- Stein, L -- Hsie, L -- Topaloglou, T -- Hubbell, E -- Robinson, E -- Mittmann, M -- Morris, M S -- Shen, N -- Kilburn, D -- Rioux, J -- Nusbaum, C -- Rozen, S -- Hudson, T J -- Lipshutz, R -- Chee, M -- Lander, E S -- HG00098/HG/NHGRI NIH HHS/ -- HG01323/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1998 May 15;280(5366):1077-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582121" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Alleles ; Chromosome Mapping/*methods ; DNA, Complementary ; Databases, Factual ; Deoxyribonucleotides/*genetics ; Dinucleoside Phosphates ; Gene Expression ; Genetic Markers ; *Genetic Techniques ; Genetic Variation ; *Genome, Human ; *Genotype ; Heterozygote ; Homozygote ; Humans ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; *Polymorphism, Genetic ; Reproducibility of Results ; Sequence Analysis, DNA ; Sequence Tagged Sites
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2008-10-18
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4765165/" 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/PMC4765165/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coller, Hilary A -- Kruglyak, Leonid -- R01 GM081686/GM/NIGMS NIH HHS/ -- R01 GM086465/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):380-1. doi: 10.1126/science.1165664.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA. hcoller@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Pair 21/*genetics/metabolism ; Disease Models, Animal ; Down Syndrome/genetics ; *Gene Expression Regulation ; Hepatocytes/*metabolism ; Histones/metabolism ; Humans ; Mice ; RNA, Messenger/genetics/metabolism ; *Regulatory Sequences, Nucleic Acid ; Species Specificity ; Transcription Factors/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 4
    Publication Date: 2009-01-20
    Description: The nematode Caenorhabditis elegans responds to pathogenic bacteria with conserved innate immune responses and pathogen avoidance behaviors. We investigated natural variation in C. elegans resistance to pathogen infection. With the use of quantitative genetic analysis, we determined that the pathogen susceptibility difference between the laboratory wild-type strain N2 and the wild isolate CB4856 is caused by a polymorphism in the npr-1 gene, which encodes a homolog of the mammalian neuropeptide Y receptor. We show that the mechanism of NPR-1-mediated pathogen resistance is through oxygen-dependent behavioral avoidance rather than direct regulation of innate immunity. For C. elegans, bacteria represent food but also a potential source of infection. Our data underscore the importance of behavioral responses to oxygen levels in finding an optimal balance between these potentially conflicting cues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748219/" 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/PMC2748219/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reddy, Kirthi C -- Andersen, Erik C -- Kruglyak, Leonid -- Kim, Dennis H -- GM071508/GM/NIGMS NIH HHS/ -- GM084477/GM/NIGMS NIH HHS/ -- HG004321/HG/NHGRI NIH HHS/ -- R01 GM084477/GM/NIGMS NIH HHS/ -- R01 GM084477-02/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-02/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jan 16;323(5912):382-4. doi: 10.1126/science.1166527.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19150845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; Caenorhabditis elegans/*genetics/immunology/*microbiology/physiology ; Caenorhabditis elegans Proteins/*genetics/*physiology ; Cues ; Genes, Helminth ; Immunity, Innate ; Movement ; Mutation ; Oxygen/physiology ; Polymorphism, Genetic ; Pseudomonas aeruginosa/*pathogenicity/physiology ; Receptors, Neuropeptide Y/*genetics/*physiology
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  • 5
    Publication Date: 2010-10-16
    Description: Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, whereas mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTLs) influencing transcript abundance traits in a cross of two Caenorhabditis elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138179/" 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/PMC3138179/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rockman, Matthew V -- Skrovanek, Sonja S -- Kruglyak, Leonid -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50 GM071508-01/GM/NIGMS NIH HHS/ -- R01 GM089972/GM/NIGMS NIH HHS/ -- R01 GM089972-02/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-01/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):372-6. doi: 10.1126/science.1194208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Center for Genomics and Systems Biology, New York University, 100 Washington Square East, New York, NY 10003, USA. mrockman@nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947766" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Caenorhabditis elegans/*genetics/physiology ; Chromosome Mapping ; Chromosomes/*genetics ; Crosses, Genetic ; Evolution, Molecular ; Gene Expression ; Genes, Helminth ; *Genetic Variation ; Logistic Models ; Models, Genetic ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Polymorphism, Single Nucleotide ; Population Density ; *Quantitative Trait Loci ; *Quantitative Trait, Heritable ; Recombination, Genetic ; *Selection, Genetic
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  • 6
    Publication Date: 2012-02-04
    Description: Resistance of nematodes to anthelmintics such as avermectins has emerged as a major global health and agricultural problem, but genes conferring natural resistance to avermectins are unknown. We show that a naturally occurring four-amino-acid deletion in the ligand-binding domain of GLC-1, the alpha-subunit of a glutamate-gated chloride channel, confers resistance to avermectins in the model nematode Caenorhabditis elegans. We also find that the same variant confers resistance to the avermectin-producing bacterium Streptomyces avermitilis. Population-genetic analyses identified two highly divergent haplotypes at the glc-1 locus that have been maintained at intermediate frequencies by long-term balancing selection. These results implicate variation in glutamate-gated chloride channels in avermectin resistance and provide a mechanism by which such resistance can be maintained.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273849/" 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/PMC3273849/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghosh, Rajarshi -- Andersen, Erik C -- Shapiro, Joshua A -- Gerke, Justin P -- Kruglyak, Leonid -- P50-GM071508/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-03/HG/NHGRI NIH HHS/ -- R01-HG004321/HG/NHGRI NIH HHS/ -- R37- MH59520/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Feb 3;335(6068):574-8. doi: 10.1126/science.1214318.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lewis-Sigler Institute for Integrative Genomics, Department of Ecology and Evolutionary Biology, and Howard Hughes Medical Institute, Princeton University, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22301316" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Antinematodal Agents/*pharmacology ; Caenorhabditis elegans/*drug effects/*genetics/physiology ; Caenorhabditis elegans Proteins/chemistry/*genetics/metabolism ; Chloride Channels/chemistry/*genetics/metabolism ; Crosses, Genetic ; Drug Resistance/genetics ; Genes, Helminth ; Genome-Wide Association Study ; Ivermectin/*analogs & derivatives/*pharmacology ; Ligands ; Molecular Sequence Data ; Mutation ; Polymorphism, Single Nucleotide ; Protein Structure, Tertiary ; Quantitative Trait Loci ; Selection, Genetic ; Streptomyces/physiology
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  • 7
    Publication Date: 2004-05-25
    Description: We used molecular markers to study genetic relationships in a diverse collection of 85 domestic dog breeds. Differences among breeds accounted for approximately 30% of genetic variation. Microsatellite genotypes were used to correctly assign 99% of individual dogs to breeds. Phylogenetic analysis separated several breeds with ancient origins from the remaining breeds with modern European origins. We identified four genetic clusters, which predominantly contained breeds with similar geographic origin, morphology, or role in human activities. These results provide a genetic classification of dog breeds and will aid studies of the genetics of phenotypic breed differences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parker, Heidi G -- Kim, Lisa V -- Sutter, Nathan B -- Carlson, Scott -- Lorentzen, Travis D -- Malek, Tiffany B -- Johnson, Gary S -- DeFrance, Hawkins B -- Ostrander, Elaine A -- Kruglyak, Leonid -- K05 CA90754/CA/NCI NIH HHS/ -- T32 HG00035/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2004 May 21;304(5674):1160-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Biology, Fred Hutchinson Cancer Research Center, Post Office Box 19024, 1100 Fairview Avenue North, D4-100, Seattle, WA 98109-1024, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15155949" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Bayes Theorem ; Biological Evolution ; *Breeding ; Computational Biology ; Dog Diseases/genetics ; Dogs/classification/*genetics ; *Genetic Variation ; *Genome ; Genotype ; *Microsatellite Repeats ; Phenotype ; Phylogeny ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; Software
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  • 8
    Publication Date: 2002-10-05
    Description: Successful propagation of the malaria parasite Plasmodium falciparum within a susceptible mosquito vector is a prerequisite for the transmission of malaria. A field-based genetic analysis of the major human malaria vector, Anopheles gambiae, has revealed natural factors that reduce the transmission of P. falciparum. Differences in P. falciparum oocyst numbers between mosquito isofemale families fed on the same infected blood indicated a large genetic component affecting resistance to the parasite, and genome-wide scanning in pedigrees of wild mosquitoes detected segregating resistance alleles. The apparently high natural frequency of resistance alleles suggests that malaria parasites (or a similar pathogen) exert a significant selective pressure on vector populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Niare, Oumou -- Markianos, Kyriacos -- Volz, Jennifer -- Oduol, Frederick -- Toure, Abdoulaye -- Bagayoko, Magaran -- Sangare, Djibril -- Traore, Sekou F -- Wang, Rui -- Blass, Claudia -- Dolo, Guimogo -- Bouare, Madama -- Kafatos, Fotis C -- Kruglyak, Leonid -- Toure, Yeya T -- Vernick, Kenneth D -- New York, N.Y. -- Science. 2002 Oct 4;298(5591):213-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Molecular Parasitology, New York University School of Medicine, 341 East 25th Street, New York, NY 10010, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12364806" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anopheles/*genetics/immunology/*parasitology/physiology ; Chromosome Mapping ; Female ; *Genes, Insect ; Genetic Linkage ; Genetic Markers ; Genome ; Genotype ; Host-Parasite Interactions ; Humans ; Insect Vectors/genetics/immunology/*parasitology/physiology ; Karyotyping ; Malaria, Falciparum/transmission ; Male ; Mali ; Oviposition ; Phenotype ; Plasmodium falciparum/pathogenicity/*physiology ; Virulence
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  • 9
    Publication Date: 1995-12-22
    Description: A physical map has been constructed of the human genome containing 15,086 sequence-tagged sites (STSs), with an average spacing of 199 kilobases. The project involved assembly of a radiation hybrid map of the human genome containing 6193 loci and incorporated a genetic linkage map of the human genome containing 5264 loci. This information was combined with the results of STS-content screening of 10,850 loci against a yeast artificial chromosome library to produce an integrated map, anchored by the radiation hybrid and genetic maps. The map provides radiation hybrid coverage of 99 percent and physical coverage of 94 percent of the human genome. The map also represents an early step in an international project to generate a transcript map of the human genome, with more than 3235 expressed sequences localized. The STSs in the map provide a scaffold for initiating large-scale sequencing of the human genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hudson, T J -- Stein, L D -- Gerety, S S -- Ma, J -- Castle, A B -- Silva, J -- Slonim, D K -- Baptista, R -- Kruglyak, L -- Xu, S H -- Hu, X -- Colbert, A M -- Rosenberg, C -- Reeve-Daly, M P -- Rozen, S -- Hui, L -- Wu, X -- Vestergaard, C -- Wilson, K M -- Bae, J S -- Maitra, S -- Ganiatsas, S -- Evans, C A -- DeAngelis, M M -- Ingalls, K A -- Nahf, R W -- Horton, L T Jr -- Anderson, M O -- Collymore, A J -- Ye, W -- Kouyoumjian, V -- Zemsteva, I S -- Tam, J -- Devine, R -- Courtney, D F -- Renaud, M T -- Nguyen, H -- O'Connor, T J -- Fizames, C -- Faure, S -- Gyapay, G -- Dib, C -- Morissette, J -- Orlin, J B -- Birren, B W -- Goodman, N -- Weissenbach, J -- Hawkins, T L -- Foote, S -- Page, D C -- Lander, E S -- HG00017/HG/NHGRI NIH HHS/ -- HG00098/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1995 Dec 22;270(5244):1945-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead-MIT Center for Genome Research, Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8533086" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Chromosome Mapping ; Chromosomes, Artificial, Yeast ; Databases, Factual ; Gene Expression ; Genetic Markers ; *Genome, Human ; *Human Genome Project ; Humans ; Hybrid Cells ; Polymerase Chain Reaction ; *Sequence Analysis, DNA ; *Sequence Tagged Sites
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2006-04-29
    Description: We surveyed an Anopheles gambiae population in a West African malaria transmission zone for naturally occurring genetic loci that control mosquito infection with the human malaria parasite, Plasmodium falciparum. The strongest Plasmodium resistance loci cluster in a small region of chromosome 2L and each locus explains at least 89% of parasite-free mosquitoes in independent pedigrees. Together, the clustered loci form a genomic Plasmodium-resistance island that explains most of the genetic variation for malaria parasite infection of mosquitoes in nature. Among the candidate genes in this chromosome region, RNA interference knockdown assays confirm a role in Plasmodium resistance for Anopheles Plasmodium-responsive leucine-rich repeat 1 (APL1), encoding a leucine-rich repeat protein that is similar to molecules involved in natural pathogen resistance mechanisms in plants and mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riehle, Michelle M -- Markianos, Kyriacos -- Niare, Oumou -- Xu, Jiannong -- Li, Jun -- Toure, Abdoulaye M -- Podiougou, Belco -- Oduol, Frederick -- Diawara, Sory -- Diallo, Mouctar -- Coulibaly, Boubacar -- Ouatara, Ahmed -- Kruglyak, Leonid -- Traore, Sekou F -- Vernick, Kenneth D -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):577-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Microbial and Plant Genomics and Department of Microbiology, University of Minnesota, St. Paul, MN 55108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645095" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anopheles gambiae/*genetics/immunology/*parasitology ; Chromosome Mapping ; Female ; *Genes, Insect ; Genetic Linkage ; Genetic Variation ; Genome, Insect ; Humans ; Immunity, Innate/genetics ; Insect Proteins/*genetics/physiology ; Insect Vectors/genetics/*parasitology ; Malaria, Falciparum/parasitology ; Male ; Mali ; Oligonucleotide Array Sequence Analysis ; Pedigree ; Phenotype ; Plasmodium berghei/immunology/pathogenicity ; Plasmodium falciparum/immunology/*pathogenicity ; RNA Interference
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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