Belinda M. Giardine

The paper identifies LDB1-dependent enhancer connectivity as critical for T-cell leukemia subtypes and reveals a metabolic vulnerability exploitable by statins.

This study uses CRISPR-Cas9 to identify EZH2 mutations that reactivate fetal hemoglobin without compromising cell fitness, showing potential for treating sickle cell disease and beta-thalassemia.

The paper identifies a novel cytoplasmic function of Def1 in yeast, showing it regulates mRNA decay and synthesis rates through interactions with post-transcriptional regulators.

This study shows SSBP3 is essential for LDB1-mediated chromatin looping and transcription, and stabilizes LDB1 homodimers.

The paper develops a framework to study variable expressivity in genetic disorders using 16p12.1 deletion models, showing how genetic background and secondary variants influence gene expression and phenotypes.

The paper compares transcriptomes and chromatin accessibility in MEP, ERY, and MEG cells to reveal divergence in gene regulation during differentiation.

This study shows LDB1 directly promotes enhancer-promoter loops and organizes multi-enhancer networks to activate transcription, independent of CTCF, cohesin, or YY1.

The paper shows that CCR4-NOT regulates gene expression and suppresses retrotransposon activation by modulating RNA decay and KZNF gene expression.

This study identifies conserved and species-specific cis-regulatory elements in human and mouse blood cells using integrative epigenomic analysis and clustering.

This study investigates genome folding in condensin-depleted mitotic chromosomes, revealing compartmentalization mechanisms distinct from interphase.

The paper shows CTCF suppresses antisense transcription at divergent promoters without affecting sense transcription, using a combination of genetic and molecular techniques.

This study investigates how CTCF and transcription influence chromatin structure reconfiguration after mitosis, revealing their distinct roles in boundary formation and gene domain establishment.

This study investigates how chromatin shearing affects ChIP-seq quality and shows that sonication levels significantly impact signal quality and specificity for different transcription factors.

S3V2-IDEAS normalizes, denoises, and integrates epigenomic data across cell types to identify epigenetic states and signal intensity patterns.

This paper introduces CLIMB, a statistical method for detecting high-dimensional associations in genomic data, showing improved precision and biological relevance in hematopoietic datasets.

The paper identifies ZNF410 as a highly specific transcriptional activator in erythroid cells that regulates CHD4 and fetal hemoglobin expression.

The paper integrates epigenomic and transcriptomic data from mouse hematopoiesis to identify regulatory elements and their dynamics across cell types.

S3norm improves normalization of epigenomic data by simultaneously adjusting sequencing depth and signal-to-noise ratio, enhancing the detection of biological variation.

The paper integrates GATA transcription factors and epigenomes in mouse hematopoietic cells using IDEAS to map regulatory landscapes and identify candidate cis-regulatory elements.

The paper examines how chromatin structures re-establish after mitosis using Hi-C, showing rapid compartment formation and dynamics of CTCF and cohesin binding.

Snapshot generates hierarchical visualizations of epigenetic features along cell differentiation hierarchies using epigenomic data from the VISION project.

The paper develops a framework to link Pol II ChIP-seq and single-cell data to transcriptional step rates, showing burst initiation and pause release are key regulated steps, while polymerase binding is not.