Bence Dániel

This study shows that inflammation-induced changes in 3D genome conformation regulate immune signal integration and transcriptional memory in macrophages.

This paper investigates the effects of Hippo pathway inhibition through pharmacological and genetic approaches, identifying kidney, pancreas, and thymus as target organs with dose-dependent toxicities.

The paper uses mtDNA mutations to trace clonal relationships of innate immune cells in cancer, showing myeloid clones are linked to monocytes and have distinct epigenetic profiles.

This study identifies phosphorylated ubiquitin (pS65Ub) as a signaling molecule that mediates mitochondrial-to-nuclear communication by modulating histone ubiquitination and gene expression in Parkinson's disease.

This study uses single-cell and spatial profiling to show that inflammatory signals from macrophages and fibroblasts drive CD8 T cell exhaustion and resistance to immune checkpoint blockade in prostate cancer.

This study identifies a SWI/SNF-targeting therapy effective against a double-negative prostate cancer subtype, showing it reduces viability in both AR-dependent and WNT-dependent models.

The paper shows IRF2 degradation by IRF1 during immune responses enhances ISG transcription, revealing a regulatory circuit between IRF1 and IRF2 in innate immunity.

Epiregulon infers single-cell TF activity using ATAC-seq and RNA-seq to predict drug response and identify drivers of cell state.

This study shows that peripheral monocytes' epigenomic landscape is rewired by a distal tumor, shaping their transcriptional response upon tumor infiltration.

The paper identifies small molecules that induce a cofactor switch in TEAD proteins from YAP to VGLL4, repressing pro-growth gene networks and showing anti-proliferative effects.

This study shows that mesothelioma cells develop drug resistance by reverting to a promoter-centric gene regulation mechanism when treated with a TEAD inhibitor.

The paper identifies a synonymous mtDNA variant that affects codon-anticodon affinity and shows its impact on cellular fitness in immune cells.

The paper develops PACER to infer clonal expansion rates from single timepoint data and identifies TCL1A activation as a mediator of clonal hematopoiesis fitness.

TCR-BERT uses self-supervised transfer learning on unlabeled T-cell receptor sequences to learn representations that improve antigen-binding prediction, specificity clustering, and computational TCR sequence design.