| TDS-C17011049-H19-pp DATASHEET Datasheet description | Download |
This primer pair specifically amplifies a genomic region from the H19 imprinting control region. The primers are thoroughly tested and optimized for routine SYBR® Green Real-Time qPCR assay following ChIP and for ChIP-sequencing library validation (e.g. before and after ChIP-seq library preparation).
| TDS-C17011049-H19-pp DATASHEET Datasheet description | Download |
| ChIP-seq grade H19 imprinting control region primer pair SDS GB en | Download |
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An ankylosing spondylitis-associated genetic variant in the IL23R-IL12RB2 intergenic region modulates enhancer activity and is associated with increased Th1-cell differentiation. |
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Functional effects were tested in luciferase reporter assays in HEK293T cells and allele-specific TF binding was investigated by electrophoretic mobility gel shift assays. IL23R and IL12RB2 mRNA levels in CD4+ T cells were compared between cases homozygous for the AS-risk 'A' allele and the protective 'G' allele. The proportions of interleukin (IL)-17A+ and interferon (IFN)-γ+ CD4+ T-cells were measured by fluorescence-activated cell sorting and compared between these AS-risk and protective genotypes.</abstracttext></p> <h4>RESULTS:</h4> <p><abstracttext label="RESULTS" nlmcategory="RESULTS">Conditional analysis identified rs11209032 as the probable causal SNP within a 1.14 kb putative enhancer between IL23R and IL12RB2. Reduced luciferase activity was seen for the risk allele (p<0.001) and reduced H3K4me1 methylation observed in CD4+ T-cells from 'A/A' homozygotes (p=0.02). The binding of nuclear extract to the risk allele was decreased ∼3.5-fold compared with the protective allele (p<0.001). The proportion of IFN-γ+ CD4+ T-cells was increased in 'A/A' homozygotes (p=0.004), but neither IL23R nor IL12RB2 mRNA was affected.</abstracttext></p> <h4>CONCLUSIONS:</h4> <p><abstracttext label="CONCLUSIONS" nlmcategory="CONCLUSIONS">The rs11209032 SNP downstream of IL23R forms part of an enhancer, allelic variation of which may influence Th1-cell numbers. Homozygosity for the risk 'A' allele is associated with more IFN-γ-secreting (Th1) cells. 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Functional effects were tested in luciferase reporter assays in HEK293T cells and allele-specific TF binding was investigated by electrophoretic mobility gel shift assays. IL23R and IL12RB2 mRNA levels in CD4+ T cells were compared between cases homozygous for the AS-risk 'A' allele and the protective 'G' allele. The proportions of interleukin (IL)-17A+ and interferon (IFN)-γ+ CD4+ T-cells were measured by fluorescence-activated cell sorting and compared between these AS-risk and protective genotypes.</abstracttext></p> <h4>RESULTS:</h4> <p><abstracttext label="RESULTS" nlmcategory="RESULTS">Conditional analysis identified rs11209032 as the probable causal SNP within a 1.14 kb putative enhancer between IL23R and IL12RB2. Reduced luciferase activity was seen for the risk allele (p<0.001) and reduced H3K4me1 methylation observed in CD4+ T-cells from 'A/A' homozygotes (p=0.02). The binding of nuclear extract to the risk allele was decreased ∼3.5-fold compared with the protective allele (p<0.001). The proportion of IFN-γ+ CD4+ T-cells was increased in 'A/A' homozygotes (p=0.004), but neither IL23R nor IL12RB2 mRNA was affected.</abstracttext></p> <h4>CONCLUSIONS:</h4> <p><abstracttext label="CONCLUSIONS" nlmcategory="CONCLUSIONS">The rs11209032 SNP downstream of IL23R forms part of an enhancer, allelic variation of which may influence Th1-cell numbers. Homozygosity for the risk 'A' allele is associated with more IFN-γ-secreting (Th1) cells. Further work is necessary to explain the mechanisms for these important observations.</abstracttext></p>', 'date' => '2016-02-25', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/26916345', 'doi' => '', 'modified' => '2016-09-27 23:14:18', 'created' => '2016-09-27 23:14:18', 'ProductsPublication' => array( 'id' => '1615', 'product_id' => '2549', 'publication_id' => '3037' ) ) $externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/26916345" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755 View::_evaluate() - CORE/Cake/View/View.php, line 971 View::_render() - CORE/Cake/View/View.php, line 933 View::render() - CORE/Cake/View/View.php, line 473 Controller::render() - CORE/Cake/Controller/Controller.php, line 963 ProductsController::slug() - APP/Controller/ProductsController.php, line 1052 ReflectionMethod::invokeArgs() - [internal], line ?? 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Functional effects were tested in luciferase reporter assays in HEK293T cells and allele-specific TF binding was investigated by electrophoretic mobility gel shift assays. IL23R and IL12RB2 mRNA levels in CD4+ T cells were compared between cases homozygous for the AS-risk 'A' allele and the protective 'G' allele. The proportions of interleukin (IL)-17A+ and interferon (IFN)-γ+ CD4+ T-cells were measured by fluorescence-activated cell sorting and compared between these AS-risk and protective genotypes.</abstracttext></p> <h4>RESULTS:</h4> <p><abstracttext label="RESULTS" nlmcategory="RESULTS">Conditional analysis identified rs11209032 as the probable causal SNP within a 1.14 kb putative enhancer between IL23R and IL12RB2. Reduced luciferase activity was seen for the risk allele (p<0.001) and reduced H3K4me1 methylation observed in CD4+ T-cells from 'A/A' homozygotes (p=0.02). The binding of nuclear extract to the risk allele was decreased ∼3.5-fold compared with the protective allele (p<0.001). The proportion of IFN-γ+ CD4+ T-cells was increased in 'A/A' homozygotes (p=0.004), but neither IL23R nor IL12RB2 mRNA was affected.</abstracttext></p> <h4>CONCLUSIONS:</h4> <p><abstracttext label="CONCLUSIONS" nlmcategory="CONCLUSIONS">The rs11209032 SNP downstream of IL23R forms part of an enhancer, allelic variation of which may influence Th1-cell numbers. Homozygosity for the risk 'A' allele is associated with more IFN-γ-secreting (Th1) cells. Further work is necessary to explain the mechanisms for these important observations.</abstracttext></p>', 'date' => '2016-02-25', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/26916345', 'doi' => '', 'modified' => '2016-09-27 23:14:18', 'created' => '2016-09-27 23:14:18', 'ProductsPublication' => array( 'id' => '1615', 'product_id' => '2549', 'publication_id' => '3037' ) ) $externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/26916345" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755 View::_evaluate() - CORE/Cake/View/View.php, line 971 View::_render() - CORE/Cake/View/View.php, line 933 View::render() - CORE/Cake/View/View.php, line 473 Controller::render() - CORE/Cake/Controller/Controller.php, line 963 ProductsController::slug() - APP/Controller/ProductsController.php, line 1052 ReflectionMethod::invokeArgs() - [internal], line ?? 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Functional effects were tested in luciferase reporter assays in HEK293T cells and allele-specific TF binding was investigated by electrophoretic mobility gel shift assays. IL23R and IL12RB2 mRNA levels in CD4+ T cells were compared between cases homozygous for the AS-risk 'A' allele and the protective 'G' allele. The proportions of interleukin (IL)-17A+ and interferon (IFN)-γ+ CD4+ T-cells were measured by fluorescence-activated cell sorting and compared between these AS-risk and protective genotypes.</abstracttext></p> <h4>RESULTS:</h4> <p><abstracttext label="RESULTS" nlmcategory="RESULTS">Conditional analysis identified rs11209032 as the probable causal SNP within a 1.14 kb putative enhancer between IL23R and IL12RB2. Reduced luciferase activity was seen for the risk allele (p<0.001) and reduced H3K4me1 methylation observed in CD4+ T-cells from 'A/A' homozygotes (p=0.02). The binding of nuclear extract to the risk allele was decreased ∼3.5-fold compared with the protective allele (p<0.001). The proportion of IFN-γ+ CD4+ T-cells was increased in 'A/A' homozygotes (p=0.004), but neither IL23R nor IL12RB2 mRNA was affected.</abstracttext></p> <h4>CONCLUSIONS:</h4> <p><abstracttext label="CONCLUSIONS" nlmcategory="CONCLUSIONS">The rs11209032 SNP downstream of IL23R forms part of an enhancer, allelic variation of which may influence Th1-cell numbers. Homozygosity for the risk 'A' allele is associated with more IFN-γ-secreting (Th1) cells. 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Functional effects were tested in luciferase reporter assays in HEK293T cells and allele-specific TF binding was investigated by electrophoretic mobility gel shift assays. IL23R and IL12RB2 mRNA levels in CD4+ T cells were compared between cases homozygous for the AS-risk 'A' allele and the protective 'G' allele. The proportions of interleukin (IL)-17A+ and interferon (IFN)-γ+ CD4+ T-cells were measured by fluorescence-activated cell sorting and compared between these AS-risk and protective genotypes.</abstracttext></p> <h4>RESULTS:</h4> <p><abstracttext label="RESULTS" nlmcategory="RESULTS">Conditional analysis identified rs11209032 as the probable causal SNP within a 1.14 kb putative enhancer between IL23R and IL12RB2. Reduced luciferase activity was seen for the risk allele (p<0.001) and reduced H3K4me1 methylation observed in CD4+ T-cells from 'A/A' homozygotes (p=0.02). The binding of nuclear extract to the risk allele was decreased ∼3.5-fold compared with the protective allele (p<0.001). The proportion of IFN-γ+ CD4+ T-cells was increased in 'A/A' homozygotes (p=0.004), but neither IL23R nor IL12RB2 mRNA was affected.</abstracttext></p> <h4>CONCLUSIONS:</h4> <p><abstracttext label="CONCLUSIONS" nlmcategory="CONCLUSIONS">The rs11209032 SNP downstream of IL23R forms part of an enhancer, allelic variation of which may influence Th1-cell numbers. Homozygosity for the risk 'A' allele is associated with more IFN-γ-secreting (Th1) cells. Further work is necessary to explain the mechanisms for these important observations.</abstracttext></p>', 'date' => '2016-02-25', 'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/26916345', 'doi' => '', 'modified' => '2016-09-27 23:14:18', 'created' => '2016-09-27 23:14:18', 'ProductsPublication' => array( 'id' => '1615', 'product_id' => '2549', 'publication_id' => '3037' ) ) $externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/26916345" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755 View::_evaluate() - CORE/Cake/View/View.php, line 971 View::_render() - CORE/Cake/View/View.php, line 933 View::render() - CORE/Cake/View/View.php, line 473 Controller::render() - CORE/Cake/Controller/Controller.php, line 963 ProductsController::slug() - APP/Controller/ProductsController.php, line 1052 ReflectionMethod::invokeArgs() - [internal], line ?? Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491 Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193 Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167 [main] - APP/webroot/index.php, line 118
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