Maya U. Sheth

The paper maps gene regulators of endothelial cell differentiation using CRISPR and single-cell RNA-seq, identifying Hippo mechanosignaling as critical for endothelial identity.

The paper identifies a compact regulatory logic governing fibroblast plasticity in fibrosis by analyzing enhancer repression and gene perturbations across multiple tissues.

This paper introduces Swap-seq, a method to systematically delete and quantify the effects of enhancers, silencers, and topological elements on gene expression in human cells.

The paper maps and redesigns the MYBPC3 promoter to enhance expression and treat haploinsufficient hypertrophic cardiomyopathy.

A web atlas counts evidence from 24 types for 188,634,118 variant-gene pairs across 50 human tissues; 1,530,420 pairs pass a high-confidence cutoff, 87% of them tissue-specific.

The paper introduces scE2G models to predict enhancer-gene regulatory interactions from single-cell data and demonstrates their performance across multiple cell types and perturbations.

The paper tests enhancer-promoter compatibility using improved assays, finding that promoter responsiveness, not enhancer rank order, determines activation sensitivity.

The paper introduces nucCAGE and PRIME to identify active cis-regulatory elements with high sensitivity and applies them to create a cell-type-resolved CRE atlas.

The paper uses a single-cell multi-omic atlas and deep learning to identify cis-regulatory elements and genetic drivers of heart development and disease.

This study identifies most distal element-gene interactions have small effect sizes (<10%) using DC-TAP-seq, revealing limitations in prior CRISPR screens and suggesting new model requirements.

This study identifies RUNX1 as a key regulator of cardiac recovery by reprogramming macrophages, showing that its inhibition promotes heart function recovery in a chronic heart failure model.

This study creates a gene regulation map of the human fetal heart to interpret genetic variants associated with congenital heart disease and cardiac traits, identifying valvular interstitial cells as key regulators.

This paper links CAD GWAS variants to causal genes in SMCs using single-cell chromatin accessibility and Hi-C data, creating a scV2E2G map for disease mechanism discovery.

This study quantifies direct interactions between 204 human activation domains and eight co-activators using a microfluidic platform, revealing 334 novel binding pairs and demonstrating the utility of analytical models for predicting activation.

This study uses CRUDO to show that cohesin and 3D contacts influence enhancer-promoter regulation, with distal enhancers showing stronger cohesin dependence.

ENCODE-rE2G, a classifier trained on K562 CRISPR perturbations, maps 13,455,443 enhancer-gene interactions across 352 biosamples, matching or exceeding prior models on CRISPR, eQTL, and GWAS benchmarks.