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VE‐cadherin N‐glycosylation modified by N‐acetylglucosaminyltransferase V regulates VE‐cadherin–β‐catenin interaction and monocyte adhesion

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What is the central question of this study? Inflammation‐induced monocyte adhesion is the initiator of most vascular diseases. The underlying mechanisms that mediate monocyte adhesion remain to be clarified fully.… Click to show full abstract

What is the central question of this study? Inflammation‐induced monocyte adhesion is the initiator of most vascular diseases. The underlying mechanisms that mediate monocyte adhesion remain to be clarified fully. What is the main finding and its importance? N‐acetylglucosaminyltransferase V (GnT‐V)‐mediated N‐glycosylation of VE‐cadherin regulates the dissociation of the VE‐cadherin–β‐catenin complex to modulate monocyte adhesion, but GnT‐V overexpression cannot rescue monocyte adhesion induced by interleukin‐1β. This study clarified the molecular mechanism of VE‐cadherin in regulating the monocyte adhesion process.

Keywords: glycosylation; adhesion; monocyte adhesion; cadherin catenin

Journal Title: Experimental Physiology
Year Published: 2021

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