Postsynaptic MT1-MMP serves as a molecular switch to synaptogenesis by clearing the surrounding ECM environment that allows effective deposition of nerve-derived synaptogenic factors to induce postsynaptic differentiation at developing NMJs.

VE-cadherin is required for trophoblast invasion of the maternal decidua and spiral arteries.

The metalloprotease ADAM10 modulates axon and synapse function by cleaving numerous synaptic and axonal membrane proteins in the central nervous system.

The modularity and unequivocal input/response of Notch signaling are harnessed to measure cell-surface shedding of diverse transmembrane receptors to identify new proteolytic switches and detect modulation of proteolysis by therapeutics.

Extracellular matrix signaling constitutively regulates cerebral blood flow in both physiological and pathological settings.

ADAM17 is a key player in the non-canonical endocytosis pathway that is used by oncogenic papillomaviruses as it allows virus/receptor platform assembly by activation of the ERK1/2 signaling pathway.

The core PCP protein acts as a internal brake to neuronal outgrowth.

EphA signaling plays dual opposite roles on axon dynamics in neurons, so it inhibits and promotes axon growth through ligand binding and receptor processing, respectively.

Macrophage production of MT1-MMP upon MI contributes to adverse cardiac remodeling and worsened function by promoting EndMT via TGFB, suggesting MT1-MMP inhibition as a therapeutic option for patients with MI.

Tracheal-derived matrix metalloproteinase 1 activity sustains tracheal branch invasion into myotubes by modulating ECM properties and dynamic behavior of sprouting tip cells.