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Alterations in NO-mediated endothelium-dependent vasodilation results in widespread vasoconstriction and coagulation abnormalities and is considered to be an early step in the development of atherosclerosis

Instead, its two Ub-binding motifs MIU1 and MIU2 are responsible for RNF168 itself accumulation at damage sites through physical interaction with RNF8-mediated ubiquitylated H2A (Doil et al

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