CCBE1 Enhances Lymphangiogenesis via A Disintegrin and Metalloprotease With Thrombospondin Motifs-3–Mediated Vascular Endothelial Growth Factor-C Activation

By M. Jeltsch, S. K. Jha, D. Tvorogov, A. Anisimov, V. Leppänen, Tanja Holopainen, R. Kivelä, Sagrario Ortega, Terhi Kärpanen, K. Alitalo. 2014

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A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “ADAMTS-3 also participates in triggering VEGFR-3 signaling, a cornerstone for the differentiation and function of lymphatic endothelial cells [129], and loss of ADAMTS-3 activity has been associated with Hennekam lymphangiectasia-lymphedema syndrome [130].”
ADAMTS proteins in human disorders (2018, background): “CCBE1 is also essential for lymphangiogenesis, and is mutated in a different form of Hennekam syndrome [32].”
The procollagen N-proteinases ADAMTS2, 3 and 14 in pathophysiology. (2015, background): “More recently, it has been shown in co-transfection studies that ADAMTS3 promotes the release of a proteolyticallycleaved active form of VEGF-C, a process that increases VEGF-R3 signaling [31].”
Extracellular matrix remodeling in tumor progression and immune escape: from mechanisms to treatments (2023, background): “Physiologically, CCBE1 promotes VEGF-C expression in a posttranslational layer to transform inactive form of VEGF-C into a mature form [448].”
Loss of ADAMTS3 activity causes Hennekam lymphangiectasia–lymphedema syndrome 3 (2017, background): “Pro-VEGFC binding to VEGFR3 is assisted by the N-terminal domain of CCBE1, but CCBE1 itself does not process VEGFC (14); rather, the cleavage is performed by ADAMTS3.”