Dieter Peter Reinhardt

This study designs a peptidomimetic inhibitor that blocks Vibrio cholerae adhesin FrhA, showing nanomolar binding affinity and reduced biofilm formation.

This study determines the structural and mechanical differences between two type V fimbriae in P. gingivalis, showing how structural tuning leads to distinct mechanical properties.

This study shows that soluble CD109 inhibits EGFR signaling and cancer stemness in HNSCC by blocking mCD109-EGFR interactions and promoting EGFR degradation.

This paper identifies Fibrillin-1 as a Notch-regulated matrix protein that maintains muscle stem cell quiescence by shielding them from mitogenic signals, and shows its loss leads to muscle dysfunction in Marfan syndrome.

The paper identifies loss-of-function variants in ADAMTS6 in patients with vascular and neurodevelopmental disorders, linking them to connective tissue defects and proposing a new syndrome called CHANS.

The paper investigates the role of elastic bending tensions in embryonic body folding, showing that ECM integrity and differential tension between tissue layers drive the process.

This paper investigates how fibronectin mutations impair chondrogenesis in skeletal dysplasia by disrupting protein secretion and causing cellular stress in mesenchymal stem cells.

This study investigates the role of fibronectin isoforms in postnatal skeletal development using knockout mice, finding that combined deletion of both isoforms leads to skeletal defects and altered chondrogenesis.

This study investigates the functional impact of SMAD3 variants in patient-derived cells, showing distinct effects of dominant negative and haploinsufficient variants on disease manifestations and age of onset.

This study shows that proteolysis of fibrillin-2 by ADAMTS6 is essential for normal skeletal development, as its absence leads to skeletal defects and reduced aggrecan and cartilage link protein.

This study generates a novel mouse model of arterial tortuosity syndrome by knocking out Slc2a10 and Gulo, revealing mitochondrial respiration defects and compromised extracellular matrix formation.