Platelet Integrins

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Platelet Integrins and Signaling

The term integrin describes an adhesion molecule family and originates from the integrative function of these molecules between extracellular ligands and the intracellular cytoskeleton (1,2). Integrins mediate cell–cell, cell–extracellular matrix, and cell–pathogen interactions. Integrins have two major functions: First, they mechanically couple the cytoskeleton to the extracellular matrix or t...

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The structure and function of platelet integrins.

Integrins are a ubiquitous family of non-covalently associated alpha/beta transmembrane heterodimers linking extracellular ligands to intracellular signaling pathways [1] [Cell, 2002; 110: 673]. Platelets contain five integrins, three beta1 integrins that mediate platelet adhesion to the matrix proteins collagen, fibronectin and laminin, and the beta3 integrins alphavbeta3 and alphaIIbbeta3 [2]...

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Platelet and osteoclast beta3 integrins are critical for bone metastasis.

Mice with a targeted deletion of beta3 integrin were used to examine the process by which tumor cells metastasize and destroy bone. Injection of B16 melanoma cells into the left cardiac ventricle resulted in osteolytic bone metastasis in 74% of beta3+/+ mice by 14 days. In contrast, only 4% of beta3-/- mice developed bone lesions. Direct intratibial inoculation of tumor resulted in marrow repla...

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Platelet integrins exhibit anisotropic mechanosensing and harness piconewton forces to mediate platelet aggregation.

Platelet aggregation at the site of vascular injury is essential in clotting. During this process, platelets are bridged by soluble fibrinogen that binds surface integrin receptors. One mystery in the mechanism of platelet aggregation pertains to how resting platelets ignore soluble fibrinogen, the third most abundant protein in the bloodstream, and yet avidly bind immobile fibrinogen on the su...

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Neutrophil-platelet adhesion: relative roles of platelet P-selectin and neutrophil beta2 (DC18) integrins.

Neutrophils and platelets interact both physically and metabolically during inflammation and thrombosis, but the mechanisms responsible for their adhesion remain incompletely understood. Neutrophil-platelet adhesion was measured after specific stimulation of neutrophils, platelets, or both and quantified by flow cytometry. Specific stimulation of either the neutrophil or the platelet led to a m...

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ژورنال

عنوان ژورنال: Japanese Journal of Thrombosis and Hemostasis

سال: 1992

ISSN: 1880-8808,0915-7441

DOI: 10.2491/jjsth.3.149