Notice (8): Undefined variable: solution_of_interest [APP/View/Products/view.ctp, line 755]Code Context<!-- BEGIN: REQUEST_FORM MODAL -->
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<p>For example, phenotypic changes observed in cancer cells are strongly linked to variations both in DNA methylation and chromatin modification patterns. Gene expression is strongly regulated by DNA methylation and chromatin dynamics; the binding sites linked to chromatin modifications are commonly integrated with transcriptomics data in order to discover the genes regulated by a specific protein. Transcriptomics data can also be integrated with open chromatin regions to accurately assess gene regulation patterns. Methylation profiles can equally be analyzed integratively with other epigenomics or transcriptomics measurements in order to understand the role of methylation with over or under expression of genes. Given the availability of different ‘omics’ data, we strongly recommend combining any of these techniques when interpreting epigenetic mechanisms.</p>
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<h2>What type of data can we combine?</h2>
<ul style="list-style-type: circle;">
<li>ChIP-Seq with methylation</li>
<li>ATAC-Seq with methylation</li>
<li>mRNA-Seq with methylation data</li>
<li>sncRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>mRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>...and more</li>
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<p>This analysis explores different linear mathematical models to estimate the relationship between two sets of omics data.</p>
<h3 class="diacol" style="font-weight: 100;">Complete analysis</h3>
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<li>List of CpGs with their methylation percentage (WGBS, RRBS, EPIC, BSAS)</li>
<li>Matrix with expression abundance estimation (total, messenger and small non-coding RNA)</li>
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<p>For example, phenotypic changes observed in cancer cells are strongly linked to variations both in DNA methylation and chromatin modification patterns. Gene expression is strongly regulated by DNA methylation and chromatin dynamics; the binding sites linked to chromatin modifications are commonly integrated with transcriptomics data in order to discover the genes regulated by a specific protein. Transcriptomics data can also be integrated with open chromatin regions to accurately assess gene regulation patterns. Methylation profiles can equally be analyzed integratively with other epigenomics or transcriptomics measurements in order to understand the role of methylation with over or under expression of genes. Given the availability of different ‘omics’ data, we strongly recommend combining any of these techniques when interpreting epigenetic mechanisms.</p>
</div>
<h2>What type of data can we combine?</h2>
<ul style="list-style-type: circle;">
<li>ChIP-Seq with methylation</li>
<li>ATAC-Seq with methylation</li>
<li>mRNA-Seq with methylation data</li>
<li>sncRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>mRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>...and more</li>
</ul>
<p>This analysis explores different linear mathematical models to estimate the relationship between two sets of omics data.</p>
<h3 class="diacol" style="font-weight: 100;">Complete analysis</h3>
<ul style="list-style-type: circle;">
<li>Summary statistics for the different technologies used</li>
<li>Trimmed and filtered reads in fastQ files after sequencing QC</li>
<li>BAM sorted files from alignment to reference genome or transcriptome (indexed bam files and bigwig files included)</li>
<li>Outcome of interest:</li>
<ul>
<li>List of peaks with their enrichment level (ChIP-Seq, ATAC-Seq, MeDIP-Seq)</li>
<li>List of CpGs with their methylation percentage (WGBS, RRBS, EPIC, BSAS)</li>
<li>Matrix with expression abundance estimation (total, messenger and small non-coding RNA)</li>
</ul>
<li>Comparative analysis aimed at finding differential responses between two groups of samples</li>
<li>Functional gene annotation on features with differential responses</li>
<li>Integration of two sets of omics data - linear regression</li>
<li>Gene ontology enrichment analysis of correlated features</li>
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$label = '<img src="/img/banners/banner-customizer-back.png" alt=""/>'include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
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View::render() - CORE/Cake/View/View.php, line 473
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Notice (8): Undefined variable: header [APP/View/Products/view.ctp, line 755]Code Context<!-- BEGIN: REQUEST_FORM MODAL -->
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<p>For example, phenotypic changes observed in cancer cells are strongly linked to variations both in DNA methylation and chromatin modification patterns. Gene expression is strongly regulated by DNA methylation and chromatin dynamics; the binding sites linked to chromatin modifications are commonly integrated with transcriptomics data in order to discover the genes regulated by a specific protein. Transcriptomics data can also be integrated with open chromatin regions to accurately assess gene regulation patterns. Methylation profiles can equally be analyzed integratively with other epigenomics or transcriptomics measurements in order to understand the role of methylation with over or under expression of genes. Given the availability of different ‘omics’ data, we strongly recommend combining any of these techniques when interpreting epigenetic mechanisms.</p>
</div>
<h2>What type of data can we combine?</h2>
<ul style="list-style-type: circle;">
<li>ChIP-Seq with methylation</li>
<li>ATAC-Seq with methylation</li>
<li>mRNA-Seq with methylation data</li>
<li>sncRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>mRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>...and more</li>
</ul>
<p>This analysis explores different linear mathematical models to estimate the relationship between two sets of omics data.</p>
<h3 class="diacol" style="font-weight: 100;">Complete analysis</h3>
<ul style="list-style-type: circle;">
<li>Summary statistics for the different technologies used</li>
<li>Trimmed and filtered reads in fastQ files after sequencing QC</li>
<li>BAM sorted files from alignment to reference genome or transcriptome (indexed bam files and bigwig files included)</li>
<li>Outcome of interest:</li>
<ul>
<li>List of peaks with their enrichment level (ChIP-Seq, ATAC-Seq, MeDIP-Seq)</li>
<li>List of CpGs with their methylation percentage (WGBS, RRBS, EPIC, BSAS)</li>
<li>Matrix with expression abundance estimation (total, messenger and small non-coding RNA)</li>
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<li>Comparative analysis aimed at finding differential responses between two groups of samples</li>
<li>Functional gene annotation on features with differential responses</li>
<li>Integration of two sets of omics data - linear regression</li>
<li>Gene ontology enrichment analysis of correlated features</li>
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<p>For example, phenotypic changes observed in cancer cells are strongly linked to variations both in DNA methylation and chromatin modification patterns. Gene expression is strongly regulated by DNA methylation and chromatin dynamics; the binding sites linked to chromatin modifications are commonly integrated with transcriptomics data in order to discover the genes regulated by a specific protein. Transcriptomics data can also be integrated with open chromatin regions to accurately assess gene regulation patterns. Methylation profiles can equally be analyzed integratively with other epigenomics or transcriptomics measurements in order to understand the role of methylation with over or under expression of genes. Given the availability of different ‘omics’ data, we strongly recommend combining any of these techniques when interpreting epigenetic mechanisms.</p>
</div>
<h2>What type of data can we combine?</h2>
<ul style="list-style-type: circle;">
<li>ChIP-Seq with methylation</li>
<li>ATAC-Seq with methylation</li>
<li>mRNA-Seq with methylation data</li>
<li>sncRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>mRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>...and more</li>
</ul>
<p>This analysis explores different linear mathematical models to estimate the relationship between two sets of omics data.</p>
<h3 class="diacol" style="font-weight: 100;">Complete analysis</h3>
<ul style="list-style-type: circle;">
<li>Summary statistics for the different technologies used</li>
<li>Trimmed and filtered reads in fastQ files after sequencing QC</li>
<li>BAM sorted files from alignment to reference genome or transcriptome (indexed bam files and bigwig files included)</li>
<li>Outcome of interest:</li>
<ul>
<li>List of peaks with their enrichment level (ChIP-Seq, ATAC-Seq, MeDIP-Seq)</li>
<li>List of CpGs with their methylation percentage (WGBS, RRBS, EPIC, BSAS)</li>
<li>Matrix with expression abundance estimation (total, messenger and small non-coding RNA)</li>
</ul>
<li>Comparative analysis aimed at finding differential responses between two groups of samples</li>
<li>Functional gene annotation on features with differential responses</li>
<li>Integration of two sets of omics data - linear regression</li>
<li>Gene ontology enrichment analysis of correlated features</li>
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Notice (8): Undefined variable: message [APP/View/Products/view.ctp, line 755]Code Context<!-- BEGIN: REQUEST_FORM MODAL -->
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<p>For example, phenotypic changes observed in cancer cells are strongly linked to variations both in DNA methylation and chromatin modification patterns. Gene expression is strongly regulated by DNA methylation and chromatin dynamics; the binding sites linked to chromatin modifications are commonly integrated with transcriptomics data in order to discover the genes regulated by a specific protein. Transcriptomics data can also be integrated with open chromatin regions to accurately assess gene regulation patterns. Methylation profiles can equally be analyzed integratively with other epigenomics or transcriptomics measurements in order to understand the role of methylation with over or under expression of genes. Given the availability of different ‘omics’ data, we strongly recommend combining any of these techniques when interpreting epigenetic mechanisms.</p>
</div>
<h2>What type of data can we combine?</h2>
<ul style="list-style-type: circle;">
<li>ChIP-Seq with methylation</li>
<li>ATAC-Seq with methylation</li>
<li>mRNA-Seq with methylation data</li>
<li>sncRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>mRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>...and more</li>
</ul>
<p>This analysis explores different linear mathematical models to estimate the relationship between two sets of omics data.</p>
<h3 class="diacol" style="font-weight: 100;">Complete analysis</h3>
<ul style="list-style-type: circle;">
<li>Summary statistics for the different technologies used</li>
<li>Trimmed and filtered reads in fastQ files after sequencing QC</li>
<li>BAM sorted files from alignment to reference genome or transcriptome (indexed bam files and bigwig files included)</li>
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<li>Matrix with expression abundance estimation (total, messenger and small non-coding RNA)</li>
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<li>ChIP-Seq with methylation</li>
<li>ATAC-Seq with methylation</li>
<li>mRNA-Seq with methylation data</li>
<li>sncRNA-Seq with ChIP-Seq or ATAC-Seq</li>
<li>mRNA-Seq with ChIP-Seq or ATAC-Seq</li>
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<h3 class="diacol" style="font-weight: 100;">Complete analysis</h3>
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<li>Trimmed and filtered reads in fastQ files after sequencing QC</li>
<li>BAM sorted files from alignment to reference genome or transcriptome (indexed bam files and bigwig files included)</li>
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<li>List of CpGs with their methylation percentage (WGBS, RRBS, EPIC, BSAS)</li>
<li>Matrix with expression abundance estimation (total, messenger and small non-coding RNA)</li>
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<li>Comparative analysis aimed at finding differential responses between two groups of samples</li>
<li>Functional gene annotation on features with differential responses</li>
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<li>ChIP-Seq with methylation</li>
<li>ATAC-Seq with methylation</li>
<li>mRNA-Seq with methylation data</li>
<li>sncRNA-Seq with ChIP-Seq or ATAC-Seq</li>
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<h3 class="diacol" style="font-weight: 100;">Complete analysis</h3>
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<li>Trimmed and filtered reads in fastQ files after sequencing QC</li>
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<li>List of CpGs with their methylation percentage (WGBS, RRBS, EPIC, BSAS)</li>
<li>Matrix with expression abundance estimation (total, messenger and small non-coding RNA)</li>
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×
