By Victor R. Preedy
This ebook covers the constitution and class of adhesion molecules with regards to signaling pathways and gene expression. It discusses immunohistochemical localization, neutrophil migration, and junctional, useful, and inflammatory adhesion molecules in pathologies resembling leukocyte decompression disease and ischemia reperfusion damage. Highlighting the clinical functions of present study, chapters disguise diabetes, weight problems, and metabolic syndrome; hypoxia; kidney ailment; smoking, atrial traumatic inflammation, and center sickness, the mind and dementia; and tumor proliferation. ultimately, it appears at molecular imaging and bioinformatics, high-throughput applied sciences, and chemotherapy.
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Extra resources for Adhesion Molecules (Modern Insights Into Disease from Molecules to Man)
As the cells migrate to their adult site, they lose 8/31/2008 3:22:15 PM 28 Adhesion Molecules the expression of N-cadherin during the migration but regain it in the final adult tissue (Hatta and Takeichi 1986, Nakagawa and Takeichi 1998). Various adhesion molecules might be required in a certain stage of development, and they disappear only to reappear in a latter stage. This requirement for adhesion molecules in the various stages of development can be easily demonstrated in the growth plate of long bones, which contains all of the stages of development in a small, confined region (Fig.
2007). Thus, JAM-A regulates proliferation but, as opposed to endothelial cells, it has a negative regulatory effect on proliferation in epithelial cells. A third line of evidence for the signaling role of JAM-A is suggested by observations that JAM-A serves as cell surface receptor for reovirus. Reovirus infection of target cells leads to activation of NF-kB and apoptosis in these cells. Interestingly, despite the ability of reovirus to infect cells in the absence of JAM-A (by binding to sialic acid residues), its ability to activate NF-kB and to induce apoptosis depends on JAM-A (Barton et al.
Nelson. 1995. Differential expression of Na+-K+-ATPase, ankyrin, fodrin, and E-cadherin along the kidney nephron. Am. J. Physiol. 269: C1417-C1432. N. C. Lazaris, M. G. Papathomas, E. Nikolakopoulou, and H. Koutselini. 2008. Altered expression of adhesion molecules in inflammatory cervical smears. Cytopathology 19: 172-178. C. C. Lamar. 2005. Cadmium nephrotoxicity is associated with a loss of N-cadherin-mediated adhesion and alterations in epithelial polarity in the proximal tubule. Toxicol. Sci.
Adhesion Molecules (Modern Insights Into Disease from Molecules to Man) by Victor R. Preedy