The University of Delaware has received a USD 1.36 million R01 research grant from the National Institute of General Medical Sciences to investigate how a family of cell-surface proteases regulates ephrin signaling, a pathway implicated in developmental defects, neurological disorders, and tumor biology. Principal investigator Shuo Wei will lead the four-year project, which runs through March 2031 under NIH grant number 1R01GM163327-01.
The work centers on ADAM-family metalloproteinases and their role in shedding class B ephrins from the cell surface in response to Eph receptor binding. While proteolytic regulation of class A ephrins has been documented, the equivalent mechanism for ephrinBs has received less attention. The grant supports two aims: characterizing how ADAM-mediated ephrinB cleavage affects downstream signaling and cell adhesion, and examining a newly identified connection between ADAM-ephrinB interactions and a branch of the beta-catenin pathway required for neuronal function. The team has already mapped ADAM cleavage sites on ephrinBs and generated uncleavable ephrinB mutants as experimental tools.
The award reflects sustained NIGMS investment in basic cell signaling research at a time when the mechanistic underpinnings of receptor-ligand regulation remain an active area of biomedical research funding. Eph receptors constitute the largest family of receptor tyrosine kinases, and their ligands, the ephrins, govern cell-cell communication across virtually every tissue type. The grant positions the University of Delaware as a site for dissecting a regulatory layer of this pathway that has direct relevance to congenital syndromes, oncology, and neuroscience.
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