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Study confirmes that the presence of functional PECAM1 on the endothelium promotes a proliferative tumor cell phenotype in vivo and in vitro. These proproliferative effects were mediated by soluble endothelialderived factors that are dependent on PECAM1 homophilic ligand interactions, but are independent of PECAM1dependent signaling.
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PECAM is required for fibronectin assembly in vascular endothelium during flow-mediated vascular remodeling.
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Differences in trafficking of CD31(+) cytotoxic T lymphocytes during acute influenza infection could modulate tolerance and contribute to a dampened adaptive immune response in neonates
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Stromal DNA replication was highly activated in the uterus of CD31(-/-) mice, manifested by upregulated cyclin series signaling and PCNA expression after E2 + P4 treatment. Collectively, CD31 inhibits E2 -mediated epithelial proliferation via recruitment and phosphorylation of SHP-2 upon receiving P4 signal in early pregnancy.
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findings suggest that PECAM-1 enhances SDF-1-induced chemotaxis by augmenting and prolonging activation of the PI3K/Akt/mTORC1 pathway and Rap1 and that PECAM-1, at least partly, exerts its activity by inhibiting SDF-1-induced internalization of CXCR4
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The data in this study provide evidence for the differential involvement of PECAM-1-ligand interactions in PECAM-1-dependent motility and the extension of filopodia.
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RrgA, binds both polymeric immunoglobulin receptor (pIgR) and PECAM-1, whereas the choline binding protein PspC binds, but to a lower extent, only pIgR
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Both the number of lung CD31-CD45-Sca-1+ cells and the expression levels of the Shh signaling pathway were downregulated in the lung tissues of mice with pulmonary emphysema. These cells and Shh signaling pathway are reactivated during acute adenovirus infection.
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In FVB/n mice, PECAM functions upstream of CD99 in leukocyte diapedesis and blocking antibodies against either molecule arrest neutrophils before they traverse the endothelium. However, in C57BL/6 mice, PECAM and CD99 appear to function at a different step, as the same antibodies arrest leukocyte migration through the endothelial basement membrane.
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These studies indicate a role for PECAM-1 in enhancing the inhibitory functions of TGF-beta in T cells
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PECAM1 acts upstream of Gab1, promoting Gab1/Akt/eNOS phosphorylation and activation, thereby confers EC responsiveness to flow.
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Radiation-induced stress conditions induce a transient accumulation of granulocytes within the liver by down-regulation/absence of PECAM-1.
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CD31 gene transfer is sufficient to recapitulate the cytoprotective mechanisms in CD31(-) pancreatic beta cells, which become resistant to immune-mediated rejection when grafted in fully allogeneic recipients
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PECAM1+ melanoma cells form vascular channels
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Data indicate that in lymphocyte specific 1 protein (LSP1)-deficient mice, PECAM-1 expression was reduced in endothelial cells, but not in neutrophils.
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Nck promoted oxidative stress-induced activation of NF-kappaB by coupling the tyrosine phosphorylation of PECAM-1 (platelet endothelial cell adhesion molecule-1) to the activation of p21-activated kinase
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PECAM-1 has a role in mediating the profibrotic and prometastasic environment caused by ethanol in endothelial cells
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the T cell co-inhibitory receptor CD31 prevents the formation of functional T/B immunological synapses and that therapeutic strategies aimed at sustaining CD31 signaling will attenuate the development of autoimmune responses in vivo.
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MMP-9 activity disrupts vascular integrity at least partially through a PECAM-1 dependent mechanism and interferes with regeneration of steatotic livers after ischemia/reperfusion injury.
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We have identified a single locus, at 35.8 Mb on murine chromosome 2, associated with PECAM-independent inflammation in the thioglycollate peritonitis (TGP) model. We suggest a name of Pitgp for this locus.
