Daniel Rico

The paper shows environmental stress more often causes loss of function than mutations, by reorganizing epigenomic topology rather than causing direct sequence damage.

The paper identifies associations between macrophage enhancers and cardiovascular disease variants using epigenomic data from immune cells.

The paper introduces a probabilistic framework to define chromatin accessibility in single-cell snATAC-seq data, avoiding arbitrary thresholds and providing a dynamic understanding of accessible regions.

This paper creates a 3D epigenomic roadmap of human B-cell differentiation, revealing regulatory mechanisms in immunity and cancer.

PLAMseq identifies genomic loci and protein interactors in a single workflow, validated for RNA polymerase II and CTCF, and applied to study histone H1 SUMOylation.

The paper analyzes gene age co-localization within TADs and finds that whole genome duplications mark a transition in gene age patterns and their association with TAD insulation and essentiality.

The paper identifies an evolutionarily conserved enhancer within the MYEOV locus that regulates CCND1 in humans and mice, suggesting a non-coding role in cancer.

Esearch3D predicts active enhancers by propagating gene expression across 3D-genome networks, showing enrichment in enhancer-associated features.

The paper identifies H3K4me3 broad domains formed by super-enhancer translocations in B-cell and T-cell malignancies, linking them to oncogene activation.

The paper uses polymer simulations to study chromatin structure changes at genomic rearrangements in B-cells and shows how these changes affect proto-oncogene expression.

The paper identifies intronic copy number variants (CNVs) as a significant source of gene expression variation in human populations, showing their association with gene expression differences and 3D genomic interactions.

The paper maps the epigenomic and functional changes during human neutrophil differentiation from bone marrow progenitors to mature cells, revealing key regulatory mechanisms.

This study compares the epigenomes of neutrophils and monocytes to identify regulatory elements and chromatin states, revealing differences in enhancer activity and DNA methylation.

The paper develops a bioinformatic workflow to classify blood epigenomes by cell type and identifies chromatin determinant regions linked to cell identity and disease.

The paper measures and compares transcriptional and epigenetic variability across immune cell types and finds neutrophils exhibit higher variability linked to immune pathways and environmental exposure.

The paper identifies 5hmC as a central hub in the chromatin network of ESCs, linking DNA demethylation to chromatin remodeling and pluripotency factors through epigenomic co-localization and co-evolution analysis.

The paper identifies higher gene expression variability in aggressive CLL subtypes and links it to clinical features like aggressiveness and therapy resistance.