cell adhesion molecule

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cell ad·he·sion mol·e·cule (CAM),

proteins that hold cells together, for example, uvomorulin, and hold them to their substrates, for example, laminin.

cell ad·he·sion mol·e·cule

(CAM) (sel ad-hē'zhŭn mol'ĕ-kyūl)
Proteins that hold cells together, e.g., uvomorulin, and hold them to their substrates, e.g., laminin.

cell adhesion molecule

,

CAM

Any molecule that traverses the cell membrane and contains a chemical domain that binds it to other cells or to the extracellular matrix.
References in periodicals archive ?
The mentioned cellular adhesion molecules play a crucial role in the migration of leucocytes from the blood to the arterial intima (transendothelial route).
Association between platelet endothelial cellular adhesion molecule 1 (PECAM-1/ CD31) polymorphisms and acute myocardial infarction: a study in patients from Sicily.
Association of circulating cellular adhesion molecules with menopausal status and hormone replacement therapy: time-dependent change in transdermal, but not oral estrogen users.
This process is mediated by cellular adhesion molecules such as sE-selectin, a specific product of endothelial cells.
36] Recent studies have examined the role of cellular adhesion molecules in tumor metastasis, but no correlation was noted in the expression or distribution of various cellular adhesion molecules by the different histologic subtypes of basal cell carcinoma.
Intercellular adhesion molecule-1 (ICAM-1) and E-, P-, and L-selectin are cellular adhesion molecules involved in the recruitment of leukocytes on the activated vessel wall during inflammation (1) and play an important role in the early stages of atherosclerosis and its complications (2).
For example, cytokines stimulate collagen synthesis in smooth muscle cells and promote endothelial and vascular smooth muscle cell activation through the induction of cellular adhesion molecules.
Because cellular adhesion molecules such as VCAM-1, intercellular adhesion molecule-1, and E-selectin and many cytokines and growth factors such as M-CSF contain functional DNA-binding sequences for NF-[kappa]B, AP-1, and egr-1, their expression is induced by the activation of these transcription factors (84).
Thus, antioxidants may protect against the development of atherosclerotis by inhibiting the activation of pro-inflammatory transcription factors that are required for the induction of cellular adhesion molecules, cytokines, and growth factors in the vessel wall.
Endothelium-derived NO inhibits the expression of cellular adhesion molecules on the endothelial surface and thereby prevents leukocyte attachment to the vessel wall (31,103).

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