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

doi:10.1126/science.aay0793

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

Community

Back to search

Article

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

Science (New York, N.Y.) - 29 Nov 2019

Nott Alexi, Holtman Inge R, Coufal Nicole G, Schlachetzki Johannes C M, Yu Miao, Hu Rong, Han Claudia Z, Pena Monique, Xiao Jiayang, Wu Yin, Keulen Zahara, Pasillas Martina P, O'Connor Carolyn, Nickl Christian K, Schafer Simon T, Shen Zeyang, Rissman Robert A, Brewer James B, Gosselin David, Gonda David D, Levy Michael L, Rosenfeld Michael G, McVicker Graham, Gage Fred H, Ren Bing, Glass Christopher K

Abstract excerpt

Noncoding genetic variation is a major driver of phenotypic diversity, but functional interpretation is challenging. To better understand common genetic variation associated with brain diseases, we defined noncoding regulatory regions for major cell types of the human brain. Whereas psychiatric disorders were primarily associated with variants in transcriptional enhancers and promoters in neurons, sporadic...

Read the complete abstract on PubMed

Topics

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

Share to Adaptor Proteins, Signal Transducing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Alzheimer Disease

Share to Chromatin

Share to Enhancer Elements, Genetic

Share to Gene Regulatory Networks

Share to Microglia

Share to Sequence Deletion

Share to Tumor Suppressor Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 31727856
DOI: 10.1126/science.aay0793
PMCID: PMC7028213

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Brain cell type-specific enhancer-promoter interactome maps and disease-risk association.PMID 31727856Read ↗

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

Integrative genomic and transcriptomic analysis identifies microglia-expressed genes with causal links to Alzheimer's disease risk.Semantic proximity Read ↗

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

Genetic risk for neurodegenerative conditions is linked to disease-specific microglial pathwaysSemantic proximity Read ↗

Genetics of the human microglia regulome refines Alzheimer’s disease risk lociSemantic proximity Read ↗

Single-nucleus multiomics reveals the disrupted regulatory programs in three brain regions of sporadic early-onset Alzheimer’s diseaseSemantic proximity Read ↗

Single-nucleus multiomics reveals the disrupted regulatory programs in three brain regions of sporadic early-onset Alzheimer's diseaseSemantic proximity Read ↗

Regulatory landscape of Alzheimer’s disease variants in human microgliaSemantic proximity Read ↗

Cell type-specific histone acetylation profiling of Alzheimer’s disease subjects and integration with geneticsSemantic proximity Read ↗

Leveraging functional annotations to map rare variants associated with Alzheimer’s disease with gruyereSemantic proximity Read ↗

Leveraging functional annotations to map rare variants associated with Alzheimer disease with gruyere.Semantic proximity Read ↗

Genome-scale transcriptional regulatory network models of psychiatric and neurodegenerative disordersSemantic proximity Read ↗

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