TL;DR: A coupling between physical adhesion and developmental signaling provides a mechanism to tightly integrate physical aspects of tissue morphogenesis with cell growth and differentiation, a coordination that is essential to achieve the intricate patterns of cells in tissues.
TL;DR: Cadherins are a family of cell adhesion receptors that are crucial for the mutual association of vertebrate cells and play a role in cell sorting mechanisms, conferring adhesion specificities on cells.
Abstract: Cadherins are a family of cell adhesion receptors that are crucial for the mutual association of vertebrate cells. Through their homophilic binding interactions, cadherins play a role in cell-sorting mechanisms, conferring adhesion specificities on cells. The regulated expression of cadherins also controls cell polarity and tissue morphology. Cadherins are thus considered to be important regulators of morphogenesis. Moreover, pathological examinations suggest that the down-regulation of cadherin expression is associated with the invasiveness of tumor cells.
TL;DR: This paper presents a meta-analyses of cDNA transference studies on CADherin FUNCTION and discusses the role of CADherins 1N MORPHOGENESIS in this research.
Abstract: PERSPECTIVES AND SUMMARY 237 SELECTIVE C LL ADHESION 238 CELL-CELL ,a,DHESION MOLECULES 239 CADHERINS 240 cDNA TRANSFECTION STUDIES ON CADHERIN FUNCTION 242 BINDING SPECIFICITIES OF CADHERINS 242 MOLECULAR BASIS FOR CADHERIN-MEDIATED SELECTIVE ADHESION ..... 244 SPECIES-SPECIFICITIES OF CADHERINS 245 TRANSMEMBRANE CONTROL OF CADHERIN FUNCTION 246 ROLE OF CADHERINS 1N MORPHOGENESIS 248
TL;DR: These studies demonstrate that CAM blockade can effectively inhibit inflammation; however, there appear to be clear differences in the adhesion requirements for particular types of inflammation.
Abstract: Neutrophil-endothelial cell interactions are mediated by interacting sets of cell adhesion molecules (CAMs) and chemoattractant/activator molecules to form an "adhesion cascade." The initial phase of inflammation, a transient slowing of neutrophils in postcapillary venules, is mediated by selectins. Subsequently, firm adhesion of neutrophils to the vessel wall occurs via interaction of the CD11/CD18 (beta 2) integrins to endothelial ligands such as intercellular adhesion molecule-1 (ICAM-1). This binding requires activation of CD11/CD18 by exposure of the neutrophil to a variety of activating/chemoattractant molecules, such as platelet-activating factor or interleukin-8. Finally, transmigration into tissues occurs, a process that requires both a chemotactic stimulus and engagement of platelet-endothelial cell adhesion molecule-1 (PECAM-1). Several approaches have been used to probe the role of CAMs in vivo. These include the use of blocking antibodies, chimeric selectin-immunoglobulin proteins, sialyl Lewisx oligosaccharides and peptides, along with the study of humans and animals with genetically determined adhesion deficiencies. These studies demonstrate that CAM blockade can effectively inhibit inflammation; however, there appear to be clear differences in the adhesion requirements for particular types of inflammation. By understanding the CAM/chemoattractant profiles involved in specific disease states, it may be possible to precisely and effectively target therapy to a wide variety of inflammatory diseases.