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However, tip cells re-express VEGFR3, and its pharmacological inhibition diminishes sprouting. In contrast,loss of VEGFR1 increases sprouting and vascularization. A soluble variant or a kinase-dead mutant of VEGFR1 rescues vascular defects caused by VEGFR1 deficiency, suggesting that this receptor functions as a VEGF trap. VEGFR1 is predominantly expressed in stalk cells and involved in guidance and limiting tip cell formation.

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