Article

Enhancer variants associated with Alzheimer’s disease affect gene expression via chromatin looping

2018-09-25

Abstract excerpt

<h4>Background:</h4> Genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms (SNPs) that may be genetic factors underlying Alzheimer’s disease (AD). However, how these AD-associated SNPs (AD SNPs) contribute to the pathogenesis of this disease is poorly understood because most of them are located in non-coding regions, such as introns and intergenic regions. Previous studies report...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 217038ab-4f4d-5589-95e8-9b90910278a9
DOI: 10.1101/426312

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Enhancer variants associated with Alzheimer’s disease affect gene expression via chromatin loopingDOI 10.1101/426312Read

Enhancer variants associated with Alzheimer’s disease affect gene expression via chromatin loopingSemantic proximity Read

Inferring the molecular mechanisms of noncoding Alzheimer’s disease-associated genetic variantsSemantic proximity Read

Cell type-specific enhancer-promoter connectivity maps in the human brain and disease risk associationSemantic proximity Read

Identification of a specific APOE transcript and functional elements associated with Alzheimer’s diseaseSemantic proximity Read

Bioinformatics strategy to advance the interpretation of Alzheimer's disease GWAS discoveries: The roads from association to causationSemantic proximity Read

Beyond association: successes and challenges in linking non-coding genetic variation to functional consequences that modulate Alzheimer's disease risk.Semantic proximity Read

Mapping Alzheimer's Disease Variants to Their Target Genes Using Computational Analysis of Chromatin Configuration.Semantic proximity Read

Brain cell type-specific enhancer-promoter interactome maps and disease-risk association.Semantic proximity Read

Single-cell epigenomic identification of inherited risk loci in Alzheimer’s and Parkinson’s diseaseSemantic proximity Read

Silencer variants are key drivers of gene upregulation in Alzheimer’s diseaseSemantic proximity Read

Deciphering the tissue-specific functional effect of Alzheimer risk SNPs with deep genome annotationSemantic proximity Read

Modeling <i>cis</i> -regulatory variation in human brain enhancers across a large Parkinson’s Disease cohortSemantic proximity Read