Andrew P. Hinck

This paper develops a method to produce highly purified inhibins using mammalian cell expression and tandem affinity purification, achieving high yields and purity with minimal activin contamination.

This paper identifies co-receptors for a parasite TGFβ antagonist, uses structural data to design cell-type-specific TGFβ modulators, and demonstrates their selective antagonistic effects.

This paper improves the folding and targeting of an engineered TGF-β monomer for gene-based delivery by modifying its pro-domain and adding a CD44 binding domain.

Conditioning RFdiffusion on edge beta-strand pairing yields specific binders to polar targets, with in silico success above 9.2% versus 0.98% for hotspot-only conditioning.

This study determines the structure of TGF-beta bound to betaglycan and its signaling receptors, revealing mechanisms of ligand selectivity and signal potentiation.

This paper shows TGM6, a helminth protein, mimics TGF-β binding to TβRII to inhibit TGF-β signaling in fibroblasts but not T cells.

This study investigates how BMP-9 and BMP-10 form disulfide bonds and dimers, showing that geometric strain, not cysteinylation, reduces dimerization propensity and that residue swaps can reverse this effect.

This paper identifies TGM4, a helminth TGF-beta mimic, as a modular ligand that selectively targets myeloid cells through specific receptor interactions, differing from TGM1's broader T cell targeting.

The paper develops an immunocompetent mouse model of Ewing sarcoma to show that TGFβ inhibition enhances immune infiltration and reduces metastasis during radiation therapy.

This paper designs high-affinity proteins that bind to convex protein sites using geometrically matching concave scaffolds, achieving low nanomolar to picomolar affinities.

The paper investigates how shear stress and low ALK1 ligand levels synergize to activate ALK1 signaling in endothelial cells, revealing kinase activity and endocytosis as critical factors.