Characterization of a Glucocorticoid Receptor Gene (GR, NR3C1) Promoter Polymorphism Reveals Functionality and Extends a Haplotype With Putative Clinical Relevance
Identifieur interne : 000543 ( PascalFrancis/Checkpoint ); précédent : 000542; suivant : 000544Characterization of a Glucocorticoid Receptor Gene (GR, NR3C1) Promoter Polymorphism Reveals Functionality and Extends a Haplotype With Putative Clinical Relevance
Auteurs : Robert Kumsta [Allemagne, Royaume-Uni] ; Dirk Moser [Allemagne] ; Fabian Streit [Allemagne] ; Jan Willem Koper [Pays-Bas] ; Jobst Meyer [Allemagne] ; Stefan Wüst [Allemagne]Source :
- American journal of medical genetics. Part B, Neuropsychiatric genetics [ 1552-4841 ] ; 2009.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis has been associated with the etiology of major depression. One of the factors underlying altered glucocorticoid signaling might be variability of the glucocorticoid receptor gene (GR, NR3C1). GR polymorphisms have been associated with variability in glucocorticoid sensitivity and endocrine responses to psychosocial stress. Furthermore, a common GR SNP (rs10482605), located in the promoter region, has been associated with major depression. We performed functional characterization of this SNP in vitro using a reporter gene assay under different stimulation conditions. Furthermore, we genotyped 219 subjects previously genotyped for four common GR SNPs to further characterize GR haplotype structure. The minor C allele of the rs10482605 SNP showed reduced transcriptional activity under unstimulated conditions and under different stimulation conditions in two brain derived cell lines. Linkage analyses revealed that the rs10482605 SNP is in high linkage disequilibrium with a A/G SNP in exon 9beta (rs6198), associated with relative glucocorticoid resistance and increased GRbeta mRNA stability. We provide evidence that two functional GR SNPs in linkage disequilibrium are responsible for both regulation of GR expression and mRNA stability. This newly characterized haplotype could increase the risk for the development of stress related disorders, including major depression. © 2008 Wiley-Liss, Inc.
Affiliations:
- Allemagne, Pays-Bas, Royaume-Uni
- Bade-Wurtemberg, District de Karlsruhe, Hollande-Méridionale, Rhénanie-Palatinat
- Mannheim, Rotterdam, Trèves (Allemagne)
- Université de Trèves
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i1="01"><s1>Institute of Psychobiology, University of Trier</s1><s2>Trier</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country><wicri:noRegion>Trier</wicri:noRegion><placeName><settlement type="city">Trèves (Allemagne)</settlement><region type="land" nuts="1">Rhénanie-Palatinat</region></placeName><orgName type="university">Université de Trèves</orgName></affiliation><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Central Institute of Mental Health</s1><s2>Mannheim</s2><s3>DEU</s3><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Mannheim</settlement></placeName></affiliation></author></analytic><series><title level="j" type="main">American journal of medical genetics. Part B, Neuropsychiatric genetics</title><title level="j" type="abbreviated">Am. j. med. genet., Part B Neuropsychiatr. genet.</title><idno type="ISSN">1552-4841</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">American journal of medical genetics. Part B, Neuropsychiatric genetics</title><title level="j" type="abbreviated">Am. j. med. genet., Part B Neuropsychiatr. genet.</title><idno type="ISSN">1552-4841</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenal glands</term><term>Axis</term><term>Characterization</term><term>Depression</term><term>Gene</term><term>Gene expression</term><term>Haplotype</term><term>Hypothalamus</term><term>Pituitary gland</term><term>Promoter</term><term>Relevance</term><term>Single nucleotide polymorphism</term><term>Stress</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Etat dépressif</term><term>Caractérisation</term><term>Gène</term><term>Promoteur</term><term>Polymorphisme mononucléotide</term><term>Haplotype</term><term>Pertinence</term><term>Expression génique</term><term>Hypothalamus</term><term>Hypophyse</term><term>Surrénale</term><term>Axe</term><term>Stress</term><term>Récepteur de glucocorticoïde</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis has been associated with the etiology of major depression. One of the factors underlying altered glucocorticoid signaling might be variability of the glucocorticoid receptor gene (GR, NR3C1). GR polymorphisms have been associated with variability in glucocorticoid sensitivity and endocrine responses to psychosocial stress. Furthermore, a common GR SNP (rs10482605), located in the promoter region, has been associated with major depression. We performed functional characterization of this SNP in vitro using a reporter gene assay under different stimulation conditions. Furthermore, we genotyped 219 subjects previously genotyped for four common GR SNPs to further characterize GR haplotype structure. The minor C allele of the rs10482605 SNP showed reduced transcriptional activity under unstimulated conditions and under different stimulation conditions in two brain derived cell lines. Linkage analyses revealed that the rs10482605 SNP is in high linkage disequilibrium with a A/G SNP in exon 9beta (rs6198), associated with relative glucocorticoid resistance and increased GRbeta mRNA stability. We provide evidence that two functional GR SNPs in linkage disequilibrium are responsible for both regulation of GR expression and mRNA stability. This newly characterized haplotype could increase the risk for the development of stress related disorders, including major depression. © 2008 Wiley-Liss, Inc.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>1552-4841</s0></fA01><fA03 i2="1"><s0>Am. j. med. genet., Part B Neuropsychiatr. genet.</s0></fA03><fA05><s2>150</s2></fA05><fA06><s2>4</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Characterization of a Glucocorticoid Receptor Gene (GR, NR3C1) Promoter Polymorphism Reveals Functionality and Extends a Haplotype With Putative Clinical Relevance</s1></fA08><fA11 i1="01" i2="1"><s1>KUMSTA (Robert)</s1></fA11><fA11 i1="02" i2="1"><s1>MOSER (Dirk)</s1></fA11><fA11 i1="03" i2="1"><s1>STREIT (Fabian)</s1></fA11><fA11 i1="04" i2="1"><s1>KOPER (Jan Willem)</s1></fA11><fA11 i1="05" i2="1"><s1>MEYER (Jobst)</s1></fA11><fA11 i1="06" i2="1"><s1>WÜST (Stefan)</s1></fA11><fA14 i1="01"><s1>Institute of Psychobiology, University of Trier</s1><s2>Trier</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="02"><s1>SGDP Centre, Institute of Psychiatry, King's College London</s1><s3>GBR</s3><sZ>1 aut.</sZ></fA14><fA14 i1="03"><s1>Central Institute of Mental Health</s1><s2>Mannheim</s2><s3>DEU</s3><sZ>6 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Internal Medicine, Erasmus MC</s1><s2>Rotterdam</s2><s3>NLD</s3><sZ>4 aut.</sZ></fA14><fA20><s1>476-482</s1></fA20><fA21><s1>2009</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>17405B</s2><s5>354000187876310030</s5></fA43><fA44><s0>0000</s0><s1>© 2009 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/2</s0></fA45><fA47 i1="01" i2="1"><s0>09-0234243</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>American journal of medical genetics. Part B, Neuropsychiatric genetics</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis has been associated with the etiology of major depression. One of the factors underlying altered glucocorticoid signaling might be variability of the glucocorticoid receptor gene (GR, NR3C1). GR polymorphisms have been associated with variability in glucocorticoid sensitivity and endocrine responses to psychosocial stress. Furthermore, a common GR SNP (rs10482605), located in the promoter region, has been associated with major depression. We performed functional characterization of this SNP in vitro using a reporter gene assay under different stimulation conditions. Furthermore, we genotyped 219 subjects previously genotyped for four common GR SNPs to further characterize GR haplotype structure. The minor C allele of the rs10482605 SNP showed reduced transcriptional activity under unstimulated conditions and under different stimulation conditions in two brain derived cell lines. Linkage analyses revealed that the rs10482605 SNP is in high linkage disequilibrium with a A/G SNP in exon 9beta (rs6198), associated with relative glucocorticoid resistance and increased GRbeta mRNA stability. We provide evidence that two functional GR SNPs in linkage disequilibrium are responsible for both regulation of GR expression and mRNA stability. This newly characterized haplotype could increase the risk for the development of stress related disorders, including major depression. © 2008 Wiley-Liss, Inc.</s0></fC01><fC02 i1="01" i2="X"><s0>002B23</s0></fC02><fC02 i1="02" i2="X"><s0>002B18C07A</s0></fC02><fC02 i1="03" i2="X"><s0>002B18C07D</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Etat dépressif</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Depression</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Estado depresivo</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Caractérisation</s0><s5>09</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Characterization</s0><s5>09</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Caracterización</s0><s5>09</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Gène</s0><s5>10</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Gene</s0><s5>10</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Gen</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Promoteur</s0><s5>11</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Promoter</s0><s5>11</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Promotor</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Polymorphisme mononucléotide</s0><s5>12</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Single nucleotide polymorphism</s0><s5>12</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Polimorfismo mononucleótido</s0><s5>12</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Haplotype</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Haplotype</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Haplotipo</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Pertinence</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Relevance</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Pertinencia</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Expression génique</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Gene expression</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Expresión genética</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Hypothalamus</s0><s5>16</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Hypothalamus</s0><s5>16</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Hipotálamo</s0><s5>16</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Hypophyse</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Pituitary gland</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Hipófisis</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Surrénale</s0><s5>18</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Adrenal glands</s0><s5>18</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Suprarrenal</s0><s5>18</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Axe</s0><s5>19</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Axis</s0><s5>19</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Eje</s0><s5>19</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Stress</s0><s5>20</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Stress</s0><s5>20</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Estrés</s0><s5>20</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Récepteur de glucocorticoïde</s0><s4>INC</s4><s5>86</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Trouble de l'humeur</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Mood disorder</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Trastorno humor</s0><s5>37</s5></fC07><fN21><s1>173</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist><affiliations><list><country><li>Allemagne</li><li>Pays-Bas</li><li>Royaume-Uni</li></country><region><li>Bade-Wurtemberg</li><li>District de Karlsruhe</li><li>Hollande-Méridionale</li><li>Rhénanie-Palatinat</li></region><settlement><li>Mannheim</li><li>Rotterdam</li><li>Trèves (Allemagne)</li></settlement><orgName><li>Université de Trèves</li></orgName></list><tree><country name="Allemagne"><region name="Rhénanie-Palatinat"><name sortKey="Kumsta, Robert" sort="Kumsta, Robert" uniqKey="Kumsta R" first="Robert" last="Kumsta">Robert Kumsta</name></region><name sortKey="Meyer, Jobst" sort="Meyer, Jobst" uniqKey="Meyer J" first="Jobst" last="Meyer">Jobst Meyer</name><name sortKey="Moser, Dirk" sort="Moser, Dirk" uniqKey="Moser D" first="Dirk" last="Moser">Dirk Moser</name><name sortKey="Streit, Fabian" sort="Streit, Fabian" uniqKey="Streit F" first="Fabian" last="Streit">Fabian Streit</name><name sortKey="Wust, Stefan" sort="Wust, Stefan" uniqKey="Wust S" first="Stefan" last="Wüst">Stefan Wüst</name><name sortKey="Wust, Stefan" sort="Wust, Stefan" uniqKey="Wust S" first="Stefan" last="Wüst">Stefan Wüst</name></country><country name="Royaume-Uni"><noRegion><name sortKey="Kumsta, Robert" sort="Kumsta, Robert" uniqKey="Kumsta R" first="Robert" last="Kumsta">Robert Kumsta</name></noRegion></country><country name="Pays-Bas"><region name="Hollande-Méridionale"><name sortKey="Koper, Jan Willem" sort="Koper, Jan Willem" uniqKey="Koper J" first="Jan Willem" last="Koper">Jan Willem Koper</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Characterization of a Glucocorticoid Receptor Gene (GR, NR3C1) Promoter Polymorphism Reveals Functionality and Extends a Haplotype With Putative Clinical Relevance
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