Raluca Gordân

The paper creates a pan-cancer catalog of mutation patterns at transcription factor binding sites across 15 tissue types, revealing enrichment in nearly one third of TF-binding site pairs.

This study quantifies intrinsic dCas9-DNA recognition using TANGO, identifying key factors affecting gRNA performance and revealing new aspects of dCas9 specificity.

The paper develops a Bayesian method to infer inheritance patterns of allelic imbalance across trios, improving ASE estimation and linking it to chromatin state and causal variants.

This study shows that UVC irradiation changes TFAM's DNA binding specificity and increases mtDNA compaction, but does not protect against DNA damage.

The paper identifies a CRISPRa gRNA with broad off-target activity that enables genome-wide transcriptional reprogramming, showing that mismatch tolerance and PAM-proximal bases determine binding specificity.

This study identifies hundreds of new cis-regulatory element-gene connections in the MHC locus using CRISPR screens and single-cell transcriptomics, revealing cell type-specific regulatory mechanisms.

This paper designs sequence-specific DNA-binding proteins computationally and validates them experimentally, achieving high specificity and affinity for target sequences.

The paper examines how divergence in intrinsically disordered regions of a eukaryotic transcription factor affects its co-TF dependence across species.

The paper investigates how DNA sequence and chromatin context influence transcription factor binding in Plasmodium falciparum, showing that both factors contribute to differential binding site selection.

The paper identifies non-recurring putative regulatory driver mutations in cancer by analyzing their effects on transcription factor-DNA binding rather than mutation recurrence.

The paper identifies sex-dependent glial-specific chromatin accessibility changes in late-onset Alzheimer's disease brains using ATAC-seq and links them to LOAD-GWAS regions.

The paper identifies intrinsic DNA-binding specificity differences between transcription factor paralogs that partly explain their distinct genomic binding patterns.

The paper quantifies incomplete gene expression and chromatin accessibility changes during MyoD-induced transdifferentiation of human fibroblasts into myoblasts, linking chromatin remodeling deficiencies to incomplete reprogramming.