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Mechanisms that regulate the function of the selectins and their ligands.
TLDR
Convincing data have been published supporting the idea that selectins and glycoprotein ligands of the selectins participate in the activation of leukocyte integrins.
Functionally specialized junctions between endothelial cells of lymphatic vessels
TLDR
It is suggested that fluid enters throughoutInitial lymphatics via openings between buttons, which open and close without disrupting junctional integrity, but most leukocytes enter the proximal half of initial lymphatics.
How leukocytes cross the vascular endothelium
TLDR
This Review focuses on recently described mechanisms that control and open exit routes for leukocytes through the endothelial barrier.
The cell polarity protein ASIP/PAR‐3 directly associates with junctional adhesion molecule (JAM)
TLDR
It is suggested that the ASIP/PAR‐3–aPKC complex is tethered to tight junctions via its association with JAM, indicating a potential role for JAM in the generation of cell polarity in epithelial cells.
Junctional adhesion molecule interacts with the PDZ domain-containing proteins AF-6 and ZO-1.
TLDR
It is suggested that JAM can be recruited to intercellular junctions by its interaction with the PDZ domain-containing proteins AF-6 and possibly ZO-1.
Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin
TLDR
Tyr685 and Tyr731 of VE-cadherin distinctly and selectively regulate the induction of vascular permeability or leukocyte extravasation in vivo.
P- and E-selectin mediate recruitment of T-helper-1 but not T-helper-2 cells into inflamed tissues
TLDR
It is shown that Th1 cells, but not Th2 cells, are able to bind to P- selectin and E-selectin, indicating that selective recruitment is an additional level of regulation for both effector function profile and character of a local immune response.
Cadherin interaction probed by atomic force microscopy.
TLDR
Higher order unbinding forces, that increase with interaction time, indicate association of cadherins into complexes with cumulative binding strength, favor a model by which the inherently weak unit binding strength and affinity of Cadherin trans-interaction requires clustering and cytoskeletal immobilization for amplification.
VE-cadherin: the major endothelial adhesion molecule controlling cellular junctions and blood vessel formation.
  • D. Vestweber
  • Biology, Medicine
    Arteriosclerosis, thrombosis, and vascular…
  • 27 December 2007
TLDR
This review will focus on recent new developments in understanding the role of VE-cadherin in controlling endothelial cell contacts and influencing endothelium cell behavior by various outside-in signaling processes.
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