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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Impact of Genetic Variants in Human Scavenger Receptor Class B Type I (<italic>SCARB1</italic>) on Plasma Lipid Traits</title><author><name sortKey="Niemsiri, Vipavee" sort="Niemsiri, Vipavee" uniqKey="Niemsiri V" first="Vipavee" last="Niemsiri">Vipavee Niemsiri</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Wang, Xingbin" sort="Wang, Xingbin" uniqKey="Wang X" first="Xingbin" last="Wang">Xingbin Wang</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Pirim, Dilek" sort="Pirim, Dilek" uniqKey="Pirim D" first="Dilek" last="Pirim">Dilek Pirim</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Radwan, Zaheda H" sort="Radwan, Zaheda H" uniqKey="Radwan Z" first="Zaheda H." last="Radwan">Zaheda H. Radwan</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Hokanson, John E" sort="Hokanson, John E" uniqKey="Hokanson J" first="John E." last="Hokanson">John E. Hokanson</name><affiliation><nlm:aff id="A2">Department of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO</nlm:aff></affiliation></author><author><name sortKey="Hamman, Richard F" sort="Hamman, Richard F" uniqKey="Hamman R" first="Richard F." last="Hamman">Richard F. Hamman</name><affiliation><nlm:aff id="A2">Department of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO</nlm:aff></affiliation></author><author><name sortKey="Barmada, M Michael" sort="Barmada, M Michael" uniqKey="Barmada M" first="M. Michael" last="Barmada">M. Michael Barmada</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Demirci, F Yesim" sort="Demirci, F Yesim" uniqKey="Demirci F" first="F. Yesim" last="Demirci">F. Yesim Demirci</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Kamboh, M Ilyas" sort="Kamboh, M Ilyas" uniqKey="Kamboh M" first="M. Ilyas" last="Kamboh">M. Ilyas Kamboh</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25245032</idno><idno type="pmc">4270916</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4270916</idno><idno type="RBID">PMC:4270916</idno><idno type="doi">10.1161/CIRCGENETICS.114.000559</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">001151</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001151</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Impact of Genetic Variants in Human Scavenger Receptor Class B Type I (<italic>SCARB1</italic>) on Plasma Lipid Traits</title><author><name sortKey="Niemsiri, Vipavee" sort="Niemsiri, Vipavee" uniqKey="Niemsiri V" first="Vipavee" last="Niemsiri">Vipavee Niemsiri</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Wang, Xingbin" sort="Wang, Xingbin" uniqKey="Wang X" first="Xingbin" last="Wang">Xingbin Wang</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Pirim, Dilek" sort="Pirim, Dilek" uniqKey="Pirim D" first="Dilek" last="Pirim">Dilek Pirim</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Radwan, Zaheda H" sort="Radwan, Zaheda H" uniqKey="Radwan Z" first="Zaheda H." last="Radwan">Zaheda H. Radwan</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Hokanson, John E" sort="Hokanson, John E" uniqKey="Hokanson J" first="John E." last="Hokanson">John E. Hokanson</name><affiliation><nlm:aff id="A2">Department of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO</nlm:aff></affiliation></author><author><name sortKey="Hamman, Richard F" sort="Hamman, Richard F" uniqKey="Hamman R" first="Richard F." last="Hamman">Richard F. Hamman</name><affiliation><nlm:aff id="A2">Department of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO</nlm:aff></affiliation></author><author><name sortKey="Barmada, M Michael" sort="Barmada, M Michael" uniqKey="Barmada M" first="M. Michael" last="Barmada">M. Michael Barmada</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Demirci, F Yesim" sort="Demirci, F Yesim" uniqKey="Demirci F" first="F. Yesim" last="Demirci">F. Yesim Demirci</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author><author><name sortKey="Kamboh, M Ilyas" sort="Kamboh, M Ilyas" uniqKey="Kamboh M" first="M. Ilyas" last="Kamboh">M. Ilyas Kamboh</name><affiliation><nlm:aff id="A1">Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</nlm:aff></affiliation></author></analytic><series><title level="j">Circulation. Cardiovascular genetics</title><idno type="ISSN">1942-325X</idno><idno type="eISSN">1942-3268</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title><p id="P1">Scavenger receptor class B type 1 (<italic>SCARB1</italic>) plays an important role in high-density lipoprotein cholesterol (HDL-C) metabolism in selective cholesteryl ester uptake and for free cholesterol cellular efflux.</p></sec><sec id="S2"><title>Methods and Results</title><p id="P2">This study aims to identify common (minor allele frequency (MAF) ≥5%) and low-frequency/rare (MAF <5%) variants, using resequencing all 13 exons and exon-intron boundaries of <italic>SCARB1</italic> in 95 individuals with extreme HDL-C levels selected from a population-based sample of 623 US non-Hispanic whites. The sequencing step identified 44 variants, of which 11 were novel with MAF <1%. Seventy-six variants (40 sequence variants, 32 common HapMap tag single nucleotide polymorphisms, and 4 relevant variants) were selected for genotyping in the total sample of 623 subjects followed by association analyses with lipid traits. Seven variants were nominally associated with apolipoprotien B (apoB) (n = 4) or HDL-C (n = 3) (<italic>P</italic> <0.05). Three variants associated with apoB remained significant after controlling false discovery rate. The most significant association was observed between rs4765615 and apoB (<italic>P</italic> = 0.0059), while rs11057844 showed the strongest association with HDL-C (<italic>P</italic> = 0.0035). A set of 17 rare variants (MAF ≤1%) showed significant association with apoB (<italic>P</italic> = 0.0284). Haplotype analysis revealed 4 regions significantly associated with either apoB or HDL-C.</p></sec><sec id="S3"><title>Conclusions</title><p id="P3">Our findings provide new information about the genetic role of <italic>SCARB1</italic> in affecting plasma apoB levels in addition to its established role in HDL-C metabolism.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">101489144</journal-id><journal-id journal-id-type="pubmed-jr-id">35623</journal-id><journal-id journal-id-type="nlm-ta">Circ Cardiovasc Genet</journal-id><journal-id journal-id-type="iso-abbrev">Circ Cardiovasc Genet</journal-id><journal-title-group><journal-title>Circulation. Cardiovascular genetics</journal-title></journal-title-group><issn pub-type="ppub">1942-325X</issn><issn pub-type="epub">1942-3268</issn></journal-meta><article-meta><article-id pub-id-type="pmid">25245032</article-id><article-id pub-id-type="pmc">4270916</article-id><article-id pub-id-type="doi">10.1161/CIRCGENETICS.114.000559</article-id><article-id pub-id-type="manuscript">NIHMS625614</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Impact of Genetic Variants in Human Scavenger Receptor Class B Type I (<italic>SCARB1</italic>) on Plasma Lipid Traits</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Niemsiri</surname><given-names>Vipavee</given-names></name><degrees>MD, MPH</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Xingbin</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Pirim</surname><given-names>Dilek</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Radwan</surname><given-names>Zaheda H.</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hokanson</surname><given-names>John E.</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Hamman</surname><given-names>Richard F.</given-names></name><degrees>MD, DrPH</degrees><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Barmada</surname><given-names>M. Michael</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Demirci</surname><given-names>F. Yesim</given-names></name><degrees>MD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Kamboh</surname><given-names>M. Ilyas</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA</aff><aff id="A2"><label>2</label>Department of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO</aff><author-notes><corresp id="CR1"><bold>Correspondence to:</bold> M. Ilyas Kamboh, Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, 130 DeSoto Street, Pittsburgh, PA 15261. Telephone: 412-624-3066. Fax: 412-624-3020, <email>kamboh@pitt.edu</email>, or F. Yesim Demirci, Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, 130 DeSoto Street, Pittsburgh, PA 15261. Telephone: 412-624-3066. Fax: 412-624-3020. <email>fyd1@pitt.edu</email>.</corresp></author-notes><pub-date pub-type="nihms-submitted"><day>20</day><month>9</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>22</day><month>9</month><year>2014</year></pub-date><pub-date pub-type="ppub"><month>12</month><year>2014</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>12</month><year>2015</year></pub-date><volume>7</volume><issue>6</issue><fpage>838</fpage><lpage>847</lpage><pmc-comment>elocation-id from pubmed: 10.1161/CIRCGENETICS.114.000559</pmc-comment>
<abstract><sec id="S1"><title>Background</title><p id="P1">Scavenger receptor class B type 1 (<italic>SCARB1</italic>) plays an important role in high-density lipoprotein cholesterol (HDL-C) metabolism in selective cholesteryl ester uptake and for free cholesterol cellular efflux.</p></sec><sec id="S2"><title>Methods and Results</title><p id="P2">This study aims to identify common (minor allele frequency (MAF) ≥5%) and low-frequency/rare (MAF <5%) variants, using resequencing all 13 exons and exon-intron boundaries of <italic>SCARB1</italic> in 95 individuals with extreme HDL-C levels selected from a population-based sample of 623 US non-Hispanic whites. The sequencing step identified 44 variants, of which 11 were novel with MAF <1%. Seventy-six variants (40 sequence variants, 32 common HapMap tag single nucleotide polymorphisms, and 4 relevant variants) were selected for genotyping in the total sample of 623 subjects followed by association analyses with lipid traits. Seven variants were nominally associated with apolipoprotien B (apoB) (n = 4) or HDL-C (n = 3) (<italic>P</italic> <0.05). Three variants associated with apoB remained significant after controlling false discovery rate. The most significant association was observed between rs4765615 and apoB (<italic>P</italic> = 0.0059), while rs11057844 showed the strongest association with HDL-C (<italic>P</italic> = 0.0035). A set of 17 rare variants (MAF ≤1%) showed significant association with apoB (<italic>P</italic> = 0.0284). Haplotype analysis revealed 4 regions significantly associated with either apoB or HDL-C.</p></sec><sec id="S3"><title>Conclusions</title><p id="P3">Our findings provide new information about the genetic role of <italic>SCARB1</italic> in affecting plasma apoB levels in addition to its established role in HDL-C metabolism.</p></sec></abstract><kwd-group><kwd>scavenger receptor class B type I</kwd><kwd>lipids</kwd><kwd>genetic variation</kwd><kwd>haplotypes</kwd><kwd>genetic association study</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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