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  • 1
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    A DOC2 protein identified by mutational profiling is essential for apicomplexan parasite exocytosis (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: Exocytosis is essential to the lytic cycle of apicomplexan parasites and required for the pathogenesis of toxoplasmosis and malaria. DOC2 proteins recruit the membrane fusion machinery required for exocytosis in a Ca(2+)-dependent fashion. Here, the phenotype of a Toxoplasma gondii conditional mutant impaired in host cell invasion and egress was pinpointed to a defect in secretion of the micronemes, an apicomplexan-specific organelle that contains adhesion proteins. Whole-genome sequencing identified the etiological point mutation in TgDOC2.1. A conditional allele of the orthologous gene engineered into Plasmodium falciparum was also defective in microneme secretion. However, the major effect was on invasion, suggesting that microneme secretion is dispensable for Plasmodium egress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3354045/" 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/PMC3354045/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farrell, Andrew -- Thirugnanam, Sivasakthivel -- Lorestani, Alexander -- Dvorin, Jeffrey D -- Eidell, Keith P -- Ferguson, David J P -- Anderson-White, Brooke R -- Duraisingh, Manoj T -- Marth, Gabor T -- Gubbels, Marc-Jan -- AI057919/AI/NIAID NIH HHS/ -- AI081220/AI/NIAID NIH HHS/ -- AI087874/AI/NIAID NIH HHS/ -- AI088314/AI/NIAID NIH HHS/ -- HG004719/HG/NHGRI NIH HHS/ -- K08 AI087874/AI/NIAID NIH HHS/ -- K08 AI087874-02/AI/NIAID NIH HHS/ -- R01 AI057919/AI/NIAID NIH HHS/ -- R01 HG004719/HG/NHGRI NIH HHS/ -- R21 AI081220/AI/NIAID NIH HHS/ -- R21 AI088314/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):218-21. doi: 10.1126/science.1210829.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Boston College, Chestnut Hill, MA 02467, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246776" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Calcium/*metabolism ; Calcium-Binding Proteins/chemistry/genetics/*metabolism ; Cell Line ; *Exocytosis ; Genes, Protozoan ; Genetic Complementation Test ; Genome, Protozoan ; Humans ; Models, Molecular ; Molecular Sequence Data ; Movement ; Mutagenesis ; Organelles/*metabolism ; Plasmodium falciparum/genetics/growth & development/physiology ; Point Mutation ; Protein Structure, Tertiary ; Protozoan Proteins/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Toxoplasma/genetics/growth & development/*physiology/ultrastructure
    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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  • 2
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    An integrated map of genetic variation from 1,092 human genomes (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-11-07
    Description: By characterizing the geographic and functional spectrum of human genetic variation, the 1000 Genomes Project aims to build a resource to help to understand the genetic contribution to disease. Here we describe the genomes of 1,092 individuals from 14 populations, constructed using a combination of low-coverage whole-genome and exome sequencing. By developing methods to integrate information across several algorithms and diverse data sources, we provide a validated haplotype map of 38 million single nucleotide polymorphisms, 1.4 million short insertions and deletions, and more than 14,000 larger deletions. We show that individuals from different populations carry different profiles of rare and common variants, and that low-frequency variants show substantial geographic differentiation, which is further increased by the action of purifying selection. We show that evolutionary conservation and coding consequence are key determinants of the strength of purifying selection, that rare-variant load varies substantially across biological pathways, and that each individual contains hundreds of rare non-coding variants at conserved sites, such as motif-disrupting changes in transcription-factor-binding sites. This resource, which captures up to 98% of accessible single nucleotide polymorphisms at a frequency of 1% in related populations, enables analysis of common and low-frequency variants in individuals from diverse, including admixed, populations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498066/" 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/PMC3498066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉1000 Genomes Project Consortium -- Abecasis, Goncalo R -- Auton, Adam -- Brooks, Lisa D -- DePristo, Mark A -- Durbin, Richard M -- Handsaker, Robert E -- Kang, Hyun Min -- Marth, Gabor T -- McVean, Gil A -- 085532/Wellcome Trust/United Kingdom -- 086084/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 095908/Wellcome Trust/United Kingdom -- AI077439/AI/NIAID NIH HHS/ -- AI2009061/AI/NIAID NIH HHS/ -- BB/I021213/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/I02593X/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- DP2OD6514/OD/NIH HHS/ -- ES015794/ES/NIEHS NIH HHS/ -- G0701805/Medical Research Council/United Kingdom -- G0801823/Medical Research Council/United Kingdom -- G0900747/Medical Research Council/United Kingdom -- G0900747(91070)/Medical Research Council/United Kingdom -- G12 MD007579/MD/NIMHD NIH HHS/ -- G12 RR003050/RR/NCRR NIH HHS/ -- HHSN268201100040C/PHS HHS/ -- HL078885/HL/NHLBI NIH HHS/ -- P01 HG004120/HG/NHGRI NIH HHS/ -- P01HG4120/HG/NHGRI NIH HHS/ -- P20 MD006899/MD/NIMHD NIH HHS/ -- P30 AG038072/AG/NIA NIH HHS/ -- P41HG2371/HG/NHGRI NIH HHS/ -- P41HG4221/HG/NHGRI NIH HHS/ -- R01 CA166661/CA/NCI NIH HHS/ -- R01 HG002898/HG/NHGRI NIH HHS/ -- R01 HG004960/HG/NHGRI NIH HHS/ -- R01 HG007022/HG/NHGRI NIH HHS/ -- R01CA166661/CA/NCI NIH HHS/ -- R01GM59290/GM/NIGMS NIH HHS/ -- R01HG2898/HG/NHGRI NIH HHS/ -- R01HG3698/HG/NHGRI NIH HHS/ -- R01HG4719/HG/NHGRI NIH HHS/ -- R01HG4960/HG/NHGRI NIH HHS/ -- R01HG5701/HG/NHGRI NIH HHS/ -- R01HL95045/HL/NHLBI NIH HHS/ -- R01MH84698/MH/NIMH NIH HHS/ -- RC2HG5552/HG/NHGRI NIH HHS/ -- RC2HG5581/HG/NHGRI NIH HHS/ -- RC2HL102925/HL/NHLBI NIH HHS/ -- RG/09/012/28096/British Heart Foundation/United Kingdom -- RG/09/12/28096/British Heart Foundation/United Kingdom -- T15 LM007056/LM/NLM NIH HHS/ -- T15LM7033/LM/NLM NIH HHS/ -- T32GM7748/GM/NIGMS NIH HHS/ -- T32GM8283/GM/NIGMS NIH HHS/ -- T32HL94284/HL/NHLBI NIH HHS/ -- U01 HG005728/HG/NHGRI NIH HHS/ -- U01 HG006513/HG/NHGRI NIH HHS/ -- U01HG5208/HG/NHGRI NIH HHS/ -- U01HG5209/HG/NHGRI NIH HHS/ -- U01HG5211/HG/NHGRI NIH HHS/ -- U01HG5214/HG/NHGRI NIH HHS/ -- U01HG5715/HG/NHGRI NIH HHS/ -- U01HG5725/HG/NHGRI NIH HHS/ -- U01HG5728/HG/NHGRI NIH HHS/ -- U01HG6513/HG/NHGRI NIH HHS/ -- U01HG6569/HG/NHGRI NIH HHS/ -- U41HG4568/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- U54HG3067/HG/NHGRI NIH HHS/ -- U54HG3079/HG/NHGRI NIH HHS/ -- U54HG3273/HG/NHGRI NIH HHS/ -- UL1 TR000124/TR/NCATS NIH HHS/ -- UL1RR024131/RR/NCRR NIH HHS/ -- WT085475/Z/08/Z/Wellcome Trust/United Kingdom -- WT085532AIA/Wellcome Trust/United Kingdom -- WT086084/Z/08/Z/Wellcome Trust/United Kingdom -- WT089250/Z/09/Z/Wellcome Trust/United Kingdom -- WT090532/Z/09/Z/Wellcome Trust/United Kingdom -- WT095552/Z/11/Z/Wellcome Trust/United Kingdom -- WT098051/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Nov 1;491(7422):56-65. doi: 10.1038/nature11632.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23128226" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Binding Sites/genetics ; Conserved Sequence/genetics ; Continental Population Groups/genetics ; Evolution, Molecular ; Genetic Variation/*genetics ; Genetics, Medical ; *Genetics, Population ; Genome, Human/*genetics ; Genome-Wide Association Study ; *Genomics ; Haplotypes/genetics ; Humans ; Nucleotide Motifs ; Polymorphism, Single Nucleotide/genetics ; Sequence Deletion/genetics ; Transcription Factors/metabolism
    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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  • 3
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    Mapping copy number variation by population-scale genome sequencing (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-02-05
    Description: Genomic structural variants (SVs) are abundant in humans, differing from other forms of variation in extent, origin and functional impact. Despite progress in SV characterization, the nucleotide resolution architecture of most SVs remains unknown. We constructed a map of unbalanced SVs (that is, copy number variants) based on whole genome DNA sequencing data from 185 human genomes, integrating evidence from complementary SV discovery approaches with extensive experimental validations. Our map encompassed 22,025 deletions and 6,000 additional SVs, including insertions and tandem duplications. Most SVs (53%) were mapped to nucleotide resolution, which facilitated analysing their origin and functional impact. We examined numerous whole and partial gene deletions with a genotyping approach and observed a depletion of gene disruptions amongst high frequency deletions. Furthermore, we observed differences in the size spectra of SVs originating from distinct formation mechanisms, and constructed a map of SV hotspots formed by common mechanisms. Our analytical framework and SV map serves as a resource for sequencing-based association studies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077050/" 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/PMC3077050/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mills, Ryan E -- Walter, Klaudia -- Stewart, Chip -- Handsaker, Robert E -- Chen, Ken -- Alkan, Can -- Abyzov, Alexej -- Yoon, Seungtai Chris -- Ye, Kai -- Cheetham, R Keira -- Chinwalla, Asif -- Conrad, Donald F -- Fu, Yutao -- Grubert, Fabian -- Hajirasouliha, Iman -- Hormozdiari, Fereydoun -- Iakoucheva, Lilia M -- Iqbal, Zamin -- Kang, Shuli -- Kidd, Jeffrey M -- Konkel, Miriam K -- Korn, Joshua -- Khurana, Ekta -- Kural, Deniz -- Lam, Hugo Y K -- Leng, Jing -- Li, Ruiqiang -- Li, Yingrui -- Lin, Chang-Yun -- Luo, Ruibang -- Mu, Xinmeng Jasmine -- Nemesh, James -- Peckham, Heather E -- Rausch, Tobias -- Scally, Aylwyn -- Shi, Xinghua -- Stromberg, Michael P -- Stutz, Adrian M -- Urban, Alexander Eckehart -- Walker, Jerilyn A -- Wu, Jiantao -- Zhang, Yujun -- Zhang, Zhengdong D -- Batzer, Mark A -- Ding, Li -- Marth, Gabor T -- McVean, Gil -- Sebat, Jonathan -- Snyder, Michael -- Wang, Jun -- Ye, Kenny -- Eichler, Evan E -- Gerstein, Mark B -- Hurles, Matthew E -- Lee, Charles -- McCarroll, Steven A -- Korbel, Jan O -- 1000 Genomes Project -- 062023/Wellcome Trust/United Kingdom -- 077009/Wellcome Trust/United Kingdom -- 077014/Wellcome Trust/United Kingdom -- 077192/Wellcome Trust/United Kingdom -- 085532/Wellcome Trust/United Kingdom -- G0701805/Medical Research Council/United Kingdom -- G1000758/Medical Research Council/United Kingdom -- P01 HG004120/HG/NHGRI NIH HHS/ -- P41 HG004221/HG/NHGRI NIH HHS/ -- P41 HG004221-01/HG/NHGRI NIH HHS/ -- P41 HG004221-02/HG/NHGRI NIH HHS/ -- P41 HG004221-03/HG/NHGRI NIH HHS/ -- P41 HG004221-03S1/HG/NHGRI NIH HHS/ -- P41 HG004221-03S2/HG/NHGRI NIH HHS/ -- P41 HG004221-03S3/HG/NHGRI NIH HHS/ -- R01 GM059290/GM/NIGMS NIH HHS/ -- R01 GM081533/GM/NIGMS NIH HHS/ -- R01 GM081533-01A1/GM/NIGMS NIH HHS/ -- R01 GM081533-02/GM/NIGMS NIH HHS/ -- R01 GM081533-03/GM/NIGMS NIH HHS/ -- R01 GM081533-04/GM/NIGMS NIH HHS/ -- R01 GM59290/GM/NIGMS NIH HHS/ -- R01 HG004719/HG/NHGRI NIH HHS/ -- R01 HG004719-01/HG/NHGRI NIH HHS/ -- R01 HG004719-02/HG/NHGRI NIH HHS/ -- R01 HG004719-02S1/HG/NHGRI NIH HHS/ -- R01 HG004719-03/HG/NHGRI NIH HHS/ -- R01 HG004719-04/HG/NHGRI NIH HHS/ -- R01 MH091350/MH/NIMH NIH HHS/ -- RC2 HG005552/HG/NHGRI NIH HHS/ -- RC2 HG005552-01/HG/NHGRI NIH HHS/ -- RC2 HG005552-02/HG/NHGRI NIH HHS/ -- U01 HG005209/HG/NHGRI NIH HHS/ -- U01 HG005209-01/HG/NHGRI NIH HHS/ -- U01 HG005209-02/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 3;470(7332):59-65. doi: 10.1038/nature09708.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21293372" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Copy Number Variations/*genetics ; Gene Duplication/genetics ; Genetic Predisposition to Disease/genetics ; *Genetics, Population ; Genome, Human/*genetics ; *Genomics ; Genotype ; Humans ; Mutagenesis, Insertional/genetics ; Reproducibility of Results ; Sequence Analysis, DNA ; Sequence Deletion/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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  • 4
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    Demographic history and rare allele sharing among human populations (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-07-05
    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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  • 5
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    Sequence Analysis and Characterization of Active Human Alu Subfamilies Based on the 1000 Genomes Pilot Project (2015)
    Oxford University Press
    Details
    Publication Date: 2015-09-24
    Description: The goal of the 1000 Genomes Consortium is to characterize human genome structural variation (SV), including forms of copy number variations such as deletions, duplications, and insertions. Mobile element insertions, particularly Alu elements, are major contributors to genomic SV among humans. During the pilot phase of the project we experimentally validated 645 (611 intergenic and 34 exon targeted) polymorphic "young" Alu insertion events, absent from the human reference genome. Here, we report high resolution sequencing of 343 (322 unique) recent Alu insertion events, along with their respective target site duplications, precise genomic breakpoint coordinates, subfamily assignment, percent divergence, and estimated A-rich tail lengths. All the sequenced Alu loci were derived from the Alu Y lineage with no evidence of retrotransposition activity involving older Alu families (e.g., Alu J and Alu S). Alu Ya5 is currently the most active Alu subfamily in the human lineage, followed by Alu Yb8, and many others including three newly identified subfamilies we have termed Alu Yb7a3, Alu Yb8b1, and Alu Ya4a1. This report provides the structural details of 322 unique Alu variants from individual human genomes collectively adding about 100 kb of genomic variation. Many Alu subfamilies are currently active in human populations, including a surprising level of Alu Y retrotransposition. Human Alu subfamilies exhibit continuous evolution with potential drivers sprouting new Alu lineages.
    Electronic ISSN: 1759-6653
    Topics: Biology
    Published by Oxford University Press
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  • 6
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    Demographic history and rare allele sharing among human populations [Genetics] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-07-20
    Description: High-throughput sequencing technology enables population-level surveys of human genomic variation. Here, we examine the joint allele frequency distributions across continental human populations and present an approach for combining complementary aspects of whole-genome, low-coverage data and targeted high-coverage data. We apply this approach to data generated by the pilot phase of the Thousand Genomes Project, including whole-genome 2–4× coverage data for 179 samples from HapMap European, Asian, and African panels as well as high-coverage target sequencing of the exons of 800 genes from 697 individuals in seven populations. We use the site frequency spectra obtained from these data to infer demographic parameters for an Out-of-Africa model for populations of African, European, and Asian descent and to predict, by a jackknife-based approach, the amount of genetic diversity that will be discovered as sample sizes are increased. We predict that the number of discovered nonsynonymous coding variants will reach 100,000 in each population after ∼1,000 sequenced chromosomes per population, whereas ∼2,500 chromosomes will be needed for the same number of synonymous variants. Beyond this point, the number of segregating sites in the European and Asian panel populations is expected to overcome that of the African panel because of faster recent population growth. Overall, we find that the majority of human genomic variable sites are rare and exhibit little sharing among diverged populations. Our results emphasize that replication of disease association for specific rare genetic variants across diverged populations must overcome both reduced statistical power because of rarity and higher population divergence.
    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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    ART: a next-generation sequencing read simulator (2012)
    Oxford University Press
    Details
    Publication Date: 2012-02-17
    Description: : ART is a set of simulation tools that generate synthetic next-generation sequencing reads. This functionality is essential for testing and benchmarking tools for next-generation sequencing data analysis including read alignment, de novo assembly and genetic variation discovery. ART generates simulated sequencing reads by emulating the sequencing process with built-in, technology-specific read error models and base quality value profiles parameterized empirically in large sequencing datasets. We currently support all three major commercial next-generation sequencing platforms: Roche's 454, Illumina's Solexa and Applied Biosystems' SOLiD. ART also allows the flexibility to use customized read error model parameters and quality profiles. Availability: Both source and binary software packages are available at http://www.niehs.nih.gov/research/resources/software/art Contact: weichun.huang@nih.gov ; gabor.marth@bc.edu Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 8
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    Genome-wide de novo risk score implicates promoter variation in autism spectrum disorder (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-12-14
    Description: Whole-genome sequencing (WGS) has facilitated the first genome-wide evaluations of the contribution of de novo noncoding mutations to complex disorders. Using WGS, we identified 255,106 de novo mutations among sample genomes from members of 1902 quartet families in which one child, but not a sibling or their parents, was affected by autism spectrum disorder (ASD). In contrast to coding mutations, no noncoding functional annotation category, analyzed in isolation, was significantly associated with ASD. Casting noncoding variation in the context of a de novo risk score across multiple annotation categories, however, did demonstrate association with mutations localized to promoter regions. We found that the strongest driver of this promoter signal emanates from evolutionarily conserved transcription factor binding sites distal to the transcription start site. These data suggest that de novo mutations in promoter regions, characterized by evolutionary and functional signatures, contribute to ASD.
    Keywords: Development, Genetics, Neuroscience, Online Only
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Scotty: a web tool for designing RNA-Seq experiments to measure differential gene expression (2013)
    Oxford University Press
    Details
    Publication Date: 2013-02-27
    Description: Motivation: A common question arises at the beginning of every experiment where RNA-Seq is used to detect differential gene expression between two conditions: How many reads should we sequence? Results: Scotty is an interactive web-based application that assists biologists to design an experiment with an appropriate sample size and read depth to satisfy the user-defined experimental objectives. This design can be based on data available from either pilot samples or publicly available datasets. Availability: Scotty can be freely accessed on the web at http://euler.bc.edu/marthlab/scotty/scotty.php Contact: gabor.marth@bc.edu Supplementary information: Supplementary data are is available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 10
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    The variant call format and VCFtools (2011)
    Oxford University Press
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    Publication Date: 2011-06-07
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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