William M. Oldham

ExplainBind predicts protein-ligand binding likelihood and identifies key residues and non-covalent interactions without structural inputs, outperforming existing methods and enabling drug discovery insights.

This study identifies alanine as a critical metabolite regulated by TGF-β that supports myofibroblast differentiation in pulmonary fibrosis through GPT2 and SLC38A2.

This study identifies subclinical liver dysfunction clusters in PAH patients and links them to pulmonary vascular resistance and immune signaling changes.

This study develops a covalent peptide targeting NEDD9-SH3 to inhibit endothelial migration and fibroproliferative remodeling in PAH by stabilizing the RT loop and modulating sulfatase-1 activity.

This study identifies LIFR as a master amplifier of fibroblast activation in IPF, showing that blocking LIFR reduces fibrosis in ex vivo tissue.

This study identifies branched chain α-ketoacids (BCKAs) as novel signaling metabolites that activate HIF1α signaling in normoxia and modulate vascular smooth muscle cell function in pulmonary vascular disease.

This study shows that the bacterial QS signal 2-AA modulates immune cell bioenergetics via the PGC-1α/ERRα axis, promoting immune tolerance and pathogen persistence.

The paper shows that metabolic rates influence developmental speed in mouse and human embryos, with mouse cells having higher metabolic rates and faster segmentation clock periods.

The paper shows that inhibiting lactate transporters MCT1 and MCT4 reduces myofibroblast differentiation and pulmonary fibrosis in vitro and in vivo.

This study develops a microfluidic method for single-cell DNA sequencing of AML tumors, revealing clonal evolution not detectable by bulk sequencing.