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Human vascular adhesion protein

Human vascular adhesion protein (HVAP) is involved in targeting lymphocytes to inflamed tissue following infection (Salmi and Jalkanen, 1997). Interestingly, the sequence of HVAP cDNA is identical to that reported for the amine oxidase from human placenta (Smith et al., 1998), and HVAP has been shown to have amine oxidase activity. The partial three dimensional structure of HVAP has been modelled based on homology to the known 3-D structure of ECAO (Salminen et at., 1998). There is an equally intriguing sequence identity between mouse vascular adhesion protein and the membrane-bound amine oxidase associated with adipoeytes (Bono et at., 1998). [Pg.221]

Houdijk WP, de Groot PG, Nievelstein PF, Sakariassen KS, Sixma U Subendothelial proteins and platelet adhesion, von Willdvand factor and fibronectin, not thrombospondin, are involv in platelet adhesion to extracellular matrix of human vascular endothelial cells. Arteriosclerosis 6 24-33,1986. [Pg.358]

The crystal structure of CuAO has been solved from Escherichia coli (ECAO), pea seedling (PSAO), Arthrobacter globiformis (AGAO), Hansetmla polymorpha (HPAO), Pichia pastoris (PPLO), " bovine serum amine oxidase (BSAO), ° and human vascular adhesion protein (VAP-1). ... [Pg.500]

Recent studies from our laboratory demonstrate an essential role for the p21 activated kinase (Pak) 1 in control of salivary gland lumen size through the cell-cell adhesion protein, E-cadherin. Pak proteins are serine-threonine kinases that control vascular integrity in zebrafish blood vessels (Buchner et al., 2007 Liu et al., 2007) and lumen formation by human endothelial cells cultured in three-dimensional collagen matrices (Koh et al., 2008 Koh et al., 2009). In the Drosophila embryonic salivary gland, Pakl functions downstream of the small... [Pg.409]

Baiillari G, Gendelman R, Gallo RC, Ensoli B (1993) The Tat protein of human immunodeficiency virus type 1, a growth factor for AIDS Kaposi sarcoma and cytokine-activated vascular cells, induces adhesion of the same cell types by using integrin receptors recognizing the ROD amino acid sequence. Proc Natl Acad Sci USA 90(17) 7941-7945... [Pg.21]

Figure 26. Reconstruction of the tunica intima on the inner surface of a clinically used polyethylene terephtalate vascular prosthesis. A non-modified inner surface of the prosthesis, B immobilization of defined assemblies of protein molecules (e.g., collagenfiarninin or collagen+fibrin) on the inner surface of the graft, C immunofluorescence of von Willebrand factor, a marker of the identity a differentiation of vascular endothelial cells, in human saphenous vein endothelial cells in cultures on the inner surface of a prosthesis coated with collagen and larninin, D detail of a layer of endothelial cells growing on a layer of collagen and fibrin. Note well developed talin-containing focal adhesion plaques. A, B conventional optical microscope, C, D confocal microscope Leica DM 2500 [30,31]. Figure 26. Reconstruction of the tunica intima on the inner surface of a clinically used polyethylene terephtalate vascular prosthesis. A non-modified inner surface of the prosthesis, B immobilization of defined assemblies of protein molecules (e.g., collagenfiarninin or collagen+fibrin) on the inner surface of the graft, C immunofluorescence of von Willebrand factor, a marker of the identity a differentiation of vascular endothelial cells, in human saphenous vein endothelial cells in cultures on the inner surface of a prosthesis coated with collagen and larninin, D detail of a layer of endothelial cells growing on a layer of collagen and fibrin. Note well developed talin-containing focal adhesion plaques. A, B conventional optical microscope, C, D confocal microscope Leica DM 2500 [30,31].
Fig. 8.1 A schematic diagram illustrating the involvement of NF-k I in gpl20, ROS, NO, PG, IL-1/3 and TNF-a-mediated neurotoxicity. NMDA-R, N-Methyl-D-aspartate receptor, cPLA2, cytosolic phospholipase A2 lyso-PtdCho, lysophosphatidylcholine AA, arachidonic acid cAMP, cyclic adenosine monophosphate PKA, protein kinase A TNF-a, tumor necrosis factor-a TNF-a-R, TNF-a-receptor IL-1/8, interleukin-1 /3 IL-l/i-R, IL-1/8-receptor, IL-6, interleukin-6 MARK, mitogen-activated protein kinase NO, nitric oxide PG, prostaglandins EP-R, prostaglandin receptors NF-kB, nuclear factor-icB NF-kB-RE, nuclear factor-/cB-response element I/cB, inhibitory subunit of NF-icB HIV-1, human immunodeficiency virus type 1 gpl20, HIV-1 coat glycoprotein COX-2, cyclooxygenase-2 iNOS, inducible nitric oxide synthase SPLA2, secretory phospholipase A2 SOD, superoxide dismutase MMP, matrix metalloproteinase and VCAM-1, vascular adhesion molecule-1... Fig. 8.1 A schematic diagram illustrating the involvement of NF-k I in gpl20, ROS, NO, PG, IL-1/3 and TNF-a-mediated neurotoxicity. NMDA-R, N-Methyl-D-aspartate receptor, cPLA2, cytosolic phospholipase A2 lyso-PtdCho, lysophosphatidylcholine AA, arachidonic acid cAMP, cyclic adenosine monophosphate PKA, protein kinase A TNF-a, tumor necrosis factor-a TNF-a-R, TNF-a-receptor IL-1/8, interleukin-1 /3 IL-l/i-R, IL-1/8-receptor, IL-6, interleukin-6 MARK, mitogen-activated protein kinase NO, nitric oxide PG, prostaglandins EP-R, prostaglandin receptors NF-kB, nuclear factor-icB NF-kB-RE, nuclear factor-/cB-response element I/cB, inhibitory subunit of NF-icB HIV-1, human immunodeficiency virus type 1 gpl20, HIV-1 coat glycoprotein COX-2, cyclooxygenase-2 iNOS, inducible nitric oxide synthase SPLA2, secretory phospholipase A2 SOD, superoxide dismutase MMP, matrix metalloproteinase and VCAM-1, vascular adhesion molecule-1...
Increases in plasma S-AA levels have previously been reported in patients with coronary disease (57). S-AA and plasma intracellular adhesion molecule-1 were elevated in patients with CAD and hyperhomocysteinemia, but only S-AA decreased after vitamin supplementation (35). Homocysteine activates nuclear factor- in endothelial cells, possibly via oxidative stress (58), and increases monocyte chemoattractant protein-1 expression in vascular smooth muscle cells (59). Additionally, it stimulates interleukin-8 expression in human endothelial cultures (60). These inflammatory factors are known to participate in the development of atherosclerosis. Taken together, these reports suggest an association of elevated tHcy and low-grade inflammation in CAD. [Pg.179]

Expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) is known to be elevated at sites of inflammation. Studies have been conducted into the effects of EGCG and TF-3 on the expression of these adhesion molecules induced by interleukin-ip (IL-lp) in cultured human umbilical vein endothelial cells (HUVECs). Both compounds significantly inhibited IL-ip-induced protein expression of VCAM and ICAM in dose-dependent manners and were associated with reduced adhesion of leukocytes to HUVECs. The m-RNA level of VCAM-1 was also inhibited by these tea polyphenolics, as was the NF-KB-dependent transcriptional activity induced by IL-lp. It is concluded that these molecules exhibit anti-inflammatory and anti-invasion properties, probably via a route involving blockage of IkB kinase. [Pg.168]

Wang, N., Verna, L., Hardy, S., Forsayeth, J., Zhu, Y., and Stemerman, M.B., Adenovirus-mediated overexpression of c-Jun and c-Fos induces intercellular adhesion molecule-1 and monocyte chemoat-tractant protein-1 in human endothelial ce]is. Arteriosclerosis, Thrombosis Vascular Biol, 19,2078-2084, 1999. [Pg.261]


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See also in sourсe #XX -- [ Pg.221 ]




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