ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors.

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A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “These observations have suggested that ADAM-10 and ADAM-17 have opposite effects on sprouting angiogenesis that may be unrelated to Notch signaling and may involve differentially expressed anti-angiogenic proteins such as TSP1 [125].”
The ADAM metalloproteinases (2008, background): “Table 6 lists several of these studies and further information can be found in the review by Ohtsu et al.”
A Disintegrin and Metalloprotease (ADAM): Historical Overview of Their Functions (2016, background): “ADAM activation by GPCRs, and the mechanisms and pathophysiological role of ADAM-dependent EGFR transactivation have been reviewed elsewhere [57,58].”
Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. (2007, background): “been identified as the metalloproteinase that promotes HB-EGF shedding (123, 140).”