Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β–dependent vascular endothelial cadherin tyrosine phosphorylation
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چکیده
This article was unintentionally published twice in this journal, by the same authors. The following should be considered the version of record and used for citation purposes: "Mehran Haidari, Wei Zhang, James T Willerson and Richard AF Dixon, Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β-dependent vascular endothelial cadherin tyrosine phosphorylation, Cardiovascular Diabetology, Volume 13, Issue 1, doi: 10.1186/1475-2840-13-112 ". The duplicate "Mehran Haidari, Wei Zhang, James T Willerson and Richard AF Dixon, Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β-dependent vascular endothelial cadherin tyrosine phosphorylation, Cardiovascular Diabetology, Volume 13, Issue 1, doi: 10.1186/1475-2840-13-105 " is to be ignored. The Publisher apologizes to the readers of the journal for not detecting the duplication during the publication process.
منابع مشابه
The tyrosine phosphatase SHP2 regulates recovery of endothelial adherens junctions through control of β-catenin phosphorylation
Impaired endothelial barrier function results in a persistent increase in endothelial permeability and vascular leakage. Repair of a dysfunctional endothelial barrier requires controlled restoration of adherens junctions, comprising vascular endothelial (VE)-cadherin and associated β-, γ-, α-, and p120-catenins. Little is known about the mechanisms by which recovery of VE-cadherin-mediated cell...
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