Chromatin architecture reveals cell type-specific target genes for kidney disease risk variants.

ABSTRACT:

Background

Cell type-specific transcriptional programming results from the combinatorial interplay between the repertoire of active regulatory elements. Disease-associated variants disrupt such programming, leading to altered expression of downstream regulated genes and the onset of pathological states. However, due to the non-linear regulatory properties of non-coding elements such as enhancers, which can activate transcription at long distances and in a non-directional way, the identification of causal variants and their target genes remains challenging. Here, we provide a multi-omics analysis to identify regulatory elements associated with functional kidney disease variants, and downstream regulated genes.

Results

In order to understand the genetic risk of kidney diseases

SUBMITTER: Duan A 

PROVIDER: S-EPMC7905576 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature