Enhancing mitochondrial Ca²⁺ uptake effectively suppresses aberrant Ca²⁺ induced arrhythmogenic events in zebrafish, mouse and human cardiomyocytes, demonstrating a critical role for mitochondria in the regulation of cardiac rhythmicity.

A functional ovarian-specific PAX8-centric regulon is susceptible to FDA-approved HDAC inhibitors, providing the rationale to target human cancers driven by lineage-survival oncogenes with epigenetic therapeutics perturbing the enhancer topology.

SF3B1-K700E, a gene mutaiton found recurrently mutated in pancreatic cancer, increases malignancy in an autochthonous mouse model of pancreatic cancer and induces resistance against TGF-β-induced apoptosis in vitro by missplicing of MAP3K7.

Class 1 histone deacetylase (HDAC) inhibitor MS-275 enhances the efficacy of glucagon-like peptide 1 receptor (GLP-1R) therapy for glycemic control and reduction of obesity.

VRAC activation, observed with a FRET sensor of intracellular LRRC8-domains movement during gating and by fluorometry, requires plasma membrane localization and diacylglycerol signaling, but is independent of intracellular ionic strength.

Viral infection can induce NKG2D ligand expression through the action of virally encoded histone deacetylase (HDAC) inhibitors, which release HDAC mediated repression of NKG2D ligands.

Genetic lineage tracing approach combined with live imaging visualized the functional stem cell activity of Doublecortin-like kinase 1⁺ cells within pancreatic cancer in vivo.

Analysis of the tumor microenvironment reveals that pancreatic tumors experience metabolic stress caused by immune cell degradation of the amino acid arginine, and that pancreatic cancers cope by synthesizing arginine to provide access this amino acid despite low tumor availability.

Fam60a, a component of the Sin3a complex, is required for embryonic development and regulates methylation at a subset of gene promoters.

Physiological and biochemical studies show that the treatment of a transgenic mouse model carrying recessive Ryr1 mutations with a combination of class II histone deacetylase inhibitors and DNA methyl transferase inhibitors significantly improves skeletal muscle function.