Bing Ren

The paper defines cardiac cell type-specific cis-regulatory elements and links disease risk variants to these elements in human hearts.

This study shows that deleting TAD boundaries in mice often causes molecular or developmental phenotypes, highlighting their importance for genome function.

SnapATAC is a software package for analyzing scATAC-seq data, revealing regulatory elements and transcriptional regulators in mouse brain cells.

The paper shows that β-catenin modulates TCF/LEF binding at gene targets, switching from inhibitory to activating complexes during nephron progenitor cell differentiation.

The paper identifies T2D risk variants in pancreatic progenitor-specific enhancers and shows their role in regulating developmental genes involved in pancreas morphogenesis.

This study shows LSD1/KDM1A suppresses primed enhancers in mESC by maintaining H3K4me1 levels and preventing aberrant enhancer activity.

This study shows that chromatin organization remains largely intact in mouse embryonic stem cells after acute CTCF depletion, despite reduced cell growth and changes in chromatin loop interactions and cohesin occupancy.

FIREcaller detects frequently interacting regions from Hi-C data and shows their association with gene regulation and GWAS variants in human tissues.

SnapHiC identifies high-resolution chromatin loops from scHi-C data and demonstrates cell-type-specific chromatin architecture in mouse and human cells.

The paper shows FOXA pioneer factors prime some enhancers but require lineage-specific TFs to activate others, influencing endodermal organ fate decisions.

The paper quantifies the mouse embryo transcriptome from E10.5 to birth using whole-tissue and single-cell RNA-seq, identifying key gene expression patterns and cell types.

The paper maps DNA methylation changes across 12 mouse tissues at 8 developmental stages, identifying methylation variant regions and tissue-specific enhancers linked to human genetic diseases.

The paper systematically maps chromatin state landscapes during mouse development by profiling histone modifications across 72 tissue-stages, identifying dynamic enhancers and transcriptional regulators.

This study investigates how CTCF binding sites mediate transcriptional insulation in mouse embryonic stem cells, showing that insulation depends on CTCF site number, sequence context, and TAD boundary location.

This study shows that CTCF depletion in mESCs weakens TAD boundaries and INs but only affects a small subset of enhancer-promoter contacts, highlighting CTCF's role in promoting long-range gene regulation.

The paper develops PETAL, a library of 62,208 mAbs against 15,199 peptides, enabling proteome-scale antibody generation and target discovery across species.

This study identifies one known and two novel genetic variants associated with heart failure through GWAS and multi-omic analyses, revealing potential causal mechanisms and shared heritability with musculoskeletal traits.

The paper develops an online learning algorithm for integrating large single-cell datasets, enabling efficient processing of millions of cells with reduced memory usage and allowing iterative refinement of cellular identity.

This study identifies DNA sequence variants that influence 3D chromatin conformation and links them to gene expression and disease risk.

The paper identifies cell type-specific enhancer-promoter connectivity in the human brain and links these to disease risk variants in Alzheimer's and psychiatric disorders.

The paper investigates chromatin architecture changes during human cardiomyocyte differentiation and identifies HERV-H retrotransposons as key regulators of TAD boundaries and gene regulation.

This paper introduces Phylo-HMRF, a probabilistic model to analyze 3D genome organization across species using Hi-C data, revealing evolutionary patterns in chromatin structure.

The paper identifies distal enhancer networks in pancreatic islets associated with type 2 diabetes risk by integrating chromatin accessibility, conformation, and genetic data.

This study identifies a large number of structural variants in human genomes using multiple sequencing technologies and presents them as a gold standard for future studies.

MAPS processes PLAC-seq and HiChIP data to identify long-range chromatin interactions by removing biases and analyzing contact frequencies.

The paper introduces Methyl-HiC, a method that simultaneously profiles DNA methylation and chromatin architecture, revealing coordinated methylation and dynamic chromatin contacts in mouse embryonic stem cells.

The paper develops a model to identify essential regulatory elements in the human genome using machine learning and validates it with functional screens.

The paper analyzes genetic diversity across 11,257 human genomes to identify context-dependent conserved regions and their association with disease variants.

The paper uses single nucleus ATAC-seq to analyze chromatin accessibility in mouse forebrain development, identifying cell-type-specific regulatory sequences and transcriptional regulators.