Valeriya Malysheva

SPARK reconstructs enhancer-based gene regulatory networks using single-cell multiomics data and prior knowledge, revealing regulatory links associated with immune disease GWAS variants.

This study shows that the FACT complex regulates cohesin dynamics on chromatin, facilitating loop extrusion and preventing cohesin accumulation in transcribed regions.

The paper investigates the chromosomal contacts of poised enhancers during the transition from naive to primed human pluripotency, revealing their dynamics and functional significance.

This study reveals a unique 3D genome architecture in premeiotic gonadal germ cells, linked to epigenetic reprogramming and loss of TADs, alongside DNA demethylation.

The paper identifies key transcription factors and regulatory elements involved in mouse gonadal sex determination through integrated transcriptomic and chromatin accessibility analyses.

This study identifies causal genes and mechanisms for juvenile idiopathic arthritis by integrating GWAS, PCHi-C, ATAC-seq, and CRISPRa/i in CD4+ T cells from JIA patients.

The paper identifies trimodal QTLs that jointly affect enhancer accessibility, promoter contacts, and gene expression in monocytes, revealing genetic links between enhancer activity and chromatin boundaries.

The paper maps promoter interactions in human ILC3s using PCHi-C and links GWAS risk variants to target genes, identifying new autoimmune disease risk genes.

The paper investigates chromosomal contacts between promoters and enhancers using Capture Hi-C, showing that cohesin depletion affects long-range contacts but not shorter-range ones.

Chicdiff detects differential chromosomal interactions in Capture Hi-C data by improving normalization and statistical methods, identifying cell type-specific interactions in human Monocytes and CD4+ T cells.

This paper introduces GRN-loop, a method combining 3D chromatin architecture with gene expression data to identify key transcription factors and DNA elements driving neural lineage commitment.