Eric Bareke

This study uses a mouse model to show that Snrpb deletion causes axial skeletal defects by disrupting p53 and RA signaling, without affecting somite patterning.

This study identifies ATR and PKMYT1 as targets to overcome carboplatin resistance in TNBC by re-sensitizing resistant models to carboplatin through mitotic catastrophe.

This study shows that H3K27M-mutant pediatric high-grade glioma cells can be reprogrammed toward a neuronal-like state using drug combinations targeting neuronal differentiation pathways.

This study investigates the role of H3K36 methylation in epigenome integrity by analyzing knockout mouse cells, revealing its impact on enhancer activity, gene body repression, and genome compartmentalization.

This study identifies IGF2 as a therapeutic target in PRC2-deficient MPNSTs by linking PRC2 loss to chromatin remodeling and activation of the IGF2-IGF2BP axis.

ChIPbinner provides an R package for analyzing broad histone marks by binning the genome into uniform windows, enabling unbiased comparison between samples and identification of differential bins.

The paper systematically perturbs H3K36 methyltransferases in mouse mesenchymal stem cells to reveal their distinct roles in H3K36 methylation states and genomic distribution.

This study investigates the etiology of craniofacial and cardiac malformations in a mouse model of SF3B4-related syndromes, identifying gene expression and splicing changes linked to developmental defects.

This study shows that Snrpb mutations cause craniofacial defects by disrupting splicing of genes involved in P53 regulation and craniofacial development.

This study investigates the epigenetic and transcriptomic effects of NSD1 mutations in head and neck squamous cell carcinoma, showing loss of H3K36me2 and DNA methylation, and gain of H3K27me3, leading to gene expression changes.

This study shows that EFTUD2 mutations cause mis-splicing of Mdm2, leading to increased P53 activity and craniofacial defects, which can be mitigated by P53 inhibitors.

This study shows TDP-43 stabilizes G3BP1 transcripts via direct binding, and TDP-43 depletion reduces G3BP1 protein levels, contributing to stress granule dysfunction in ALS/FTD.