Selectin-carbohydrate interactions during inflammation and metastasis

L-, E-, and P-selectin are membrane-anchored, C-type lectins that initiate tethering and rolling of flowing leukocytes on endothelial cells, platelets, or other leukocytes during inflammation. The selectins bind to sialylated, fucosylated, or, in some cases, sulfated glycans on glycoproteins, glycol...

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Bibliographic Details
Published in:Glycoconjugate journal 1997-08, Vol.14 (5), p.585-591
Main Author: McEver, R P
Format: Article
Language:English
Subjects:
Blood Platelets - physiology
Carbohydrate Sequence
E-Selectin - physiology
Endothelium, Vascular - physiology
Fucose
Glycoconjugates - physiology
Humans
Inflammation - pathology
Inflammation - physiopathology
L-Selectin - physiology
Leukocytes
Leukocytes - physiology
Molecular Sequence Data
Neoplasm Metastasis - pathology
Neoplasm Metastasis - physiopathology
Neoplasms - physiopathology
Oligosaccharides - chemistry
Oligosaccharides - metabolism
P-Selectin - physiology
Selectins - physiology
Sialic Acids
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Description
Summary:L-, E-, and P-selectin are membrane-anchored, C-type lectins that initiate tethering and rolling of flowing leukocytes on endothelial cells, platelets, or other leukocytes during inflammation. The selectins bind to sialylated, fucosylated, or, in some cases, sulfated glycans on glycoproteins, glycolipids, or proteoglycans. However, they bind with relatively high affinity or avidity to only a few, appropriately modified glycoproteins on leukocytes or endothelial cells. One leukocyte mucin, PSGL-1, tethers flowing leukocytes to P-selectin on activated platelets or endothelial cells, and also helps tether leukocytes to L-selectin on other leukocytes. The physiologic expression of the selectins is tightly controlled to limit the inflammatory response. But dysregulated expression of the selectins may contribute to inflammatory and thrombotic disorders, and perhaps to tumor metastases.
ISSN:0282-0080
1573-4986
DOI:10.1023/a:1018584425879