Cloning of the mouse endothelial selectins. Expression of both E- and P-selectin is inducible by tumor necrosis factor alpha.

摘要: E-selectin (ELAM-1) and P-selectin (GMP-140, PADGEM, CD62) have both been described as human endothelial cell adhesion molecules for neutrophils monocytes. Cell surface appearance of these two proteins on umbilical vein cells can be regulated by different mechanisms: is transcriptionally induced, within hours, tumor necrosis factor alpha (TNF-alpha) while transported from storage granules to the plasma membrane minutes upon induction various stimulating agents. We obtained cDNA clones covering full-length coding sequence homologous mouse selectins. show that synthesis P-selectin, like E-selectin, transiently induced TNF-alpha in several endothelioma lines derived tissues. This was monitored RNA well protein level. The TNF newly synthesized detected surface. Protein expression increased with a slightly lower rate than E-selectin. In organ cultures lung tissue TNF-injected mice, clearly elevated compared control mice. bovine homolog recognized cross-reaction anti-mouse antibodies also TNF-inducible primary capillary adrenal cortex aorta-derived cells. Thus, levels. While transport stored controlled secretion granules, similarly