Angiomotin-like protein 1 (AMOTL1)

Angiomotin-like protein 1 (AMOTL1) is a peripheral membrane and scaffolding protein of the angiomotin family critically involved in regulating cell–cell junctions, cytoskeletal dynamics, and endothelial cell polarity[1][4][7][10]. AMOTL1 is an effector at tight and adherens junctions, binding key molecules like YAP/TAZ to restrict their nuclear activity within the Hippo signaling pathway, thereby modulating cell proliferation and apoptosis[1][5]. It is essential for angiogenesis, vascular remodeling, and normal morphogenesis, functioning by associating with N-cadherin and integrating adhesive and cytoskeletal signals during endothelial and epithelial organization[6][7]. Germline mutations in AMOTL1 have been identified as causative in a novel syndromic orofacial clefting disorder, typically with variable penetrance and phenotypes ranging from isolated cleft lip/palate to multi-organ disease[3]. Although AMOTL1 is not currently a direct therapeutic target and there are no known drugs acting on it, altered function is associated with cancer progression—especially by impacting YAP1 stability in gastric cancer[5][8]. Its biological and pathological significance lies in junctional integrity, tissue morphogenesis, and control of proliferation through the Hippo pathway.

Other names

Angiomotin-like protein 1AMOTL1JEAPJunction-enriched and associated proteinCFCHS