ADAM15 regulates endothelial permeability and neutrophil migration via Src/ERK1/2 signalling.

By ChongXiu Sun, Mack H. Wu, M. Guo, M. Day, Eugene S. Lee, S. Yuan. 2010

88 citations recorded by the source corpus.

Subfields: Immunology and Allergy, Molecular Biology, Oncology

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology and Allergy

1. S. Zhong
2. R. Khalil

In Molecular Biology

1. Carlos Fernandez-Patron
2. S. Zhong
3. Pu Zhang
4. R. Khalil
5. Mengcheng Shen
6. Z. Kassiri

In Oncology

1. S. Zhong
2. Carlos Fernandez-Patron
3. Pu Zhang
4. R. Khalil
5. Mengcheng Shen
6. Z. Kassiri

Citations in the corpus

• A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “By activation of Src kinase, phosphorylation of ERK1/2 and cleaving E-cadherin, ADAM-15 decreases the stability of endothelial cells thus promoting endothelial cell permeability, neutrophil transendothelial migration and inflammatory cell infiltration [78].”
• ADAMs family and relatives in cardiovascular physiology and pathology. (2016, background): “ADAM15 has been reported to increase endothelial permeability thereby promoting neutrophil transendothelial migration and inflammation, not by directly cleaving the endothelial cadherin in the arteries, but through activation of Src kinase and phosphorylation of ERK1/2 [80].”
• ADAM15 contributes to atherosclerosis by mediating endothelial barrier dysfunction via Src family kinase activity (2012, background): “Recently, our own investigations have implicated ADAM15 in endothelial barrier dysfunction.(18) In the present study, we provide novel evidence for a pathogenic role of ADAM15 in chronic vascular inflammation in a mouse model of atherosclerosis.”