Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Missing Regulation Between Genetic Association and Transcriptional Abundance for Hypercholesterolemia Genes.

Genes - 15 Jan 2025

Hakim Aaron, Connally Noah J, Schnitzler Gavin R, Cho Michael H, Jiang Z Gordon, Sunyaev Shamil R, Gupta Rajat M

Abstract excerpt

Background: Low-density lipoprotein cholesterol (LDL-C) is a well-established risk factor for cardiovascular disease, and it plays a causal role in the development of atherosclerosis. Genome-wide association studies (GWASs) have successfully identified hundreds of genetic variants associated with LDL-C. Most of these risk loci fall in non-coding regions of the genome, and it is unclear how these non-coding...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cholesterol, LDL
Share to Gene Expression Regulation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genetic Predisposition to Disease

Share to Genome-Wide Association Study

Share to Hypercholesterolemia

Share to Polymorphism, Single Nucleotide

Share to Quantitative Trait Loci

Source

Open in PubMed Open full text

Identifiers

PMID: 39858631
DOI: 10.3390/genes16010084
PMCID: PMC11764661

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Missing Regulation Between Genetic Association and Transcriptional Abundance for Hypercholesterolemia Genes.PMID 39858631Read ↗

Integration of genetic colocalizations with physiological and pharmacological perturbations identifies cardiometabolic disease genesSemantic proximity Read ↗

Insights Into Causal Effects of Genetically Proxied Lipids and Lipid-Modifying Drug Targets on Cardiometabolic Diseases.Semantic proximity Read ↗

Systematic Integration of genomics with transcriptomics for the Study of Coronary Artery Disease and Subclinical AtherosclerosisSemantic proximity Read ↗

A multi-layer functional genomic analysis to understand noncoding genetic variation in lipids.Semantic proximity Read ↗

Single-cell transcriptome-wide Mendelian randomization and colocalization analyses uncover cell-specific mechanisms in atherosclerotic cardiovascular diseaseSemantic proximity Read ↗

Liver eQTL meta-analysis illuminates potential molecular mechanisms of cardiometabolic traits.Semantic proximity Read ↗

The missing link between genetic association and regulatory function.Semantic proximity Read ↗

Single-cell transcriptome-wide Mendelian randomization and colocalization analyses uncover cell-specific mechanisms in atherosclerotic cardiovascular disease.Semantic proximity Read ↗

Genetic associations with expression for genes implicated in GWAS studies for atherosclerotic cardiovascular disease and blood phenotypes.Semantic proximity Read ↗

Higher eQTL power reveals signals that boost GWAS colocalizationSemantic proximity Read ↗

Integrated genome-wide analysis of expression quantitative trait loci aids interpretation of genomic association studies.Semantic proximity Read ↗

A mega-analysis of expression quantitative trait loci (eQTL) provides insight into the regulatory architecture of gene expression variation in liver.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.