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Smooth muscle antibody

A wide selection of monoclonal and polyclonal anti-Ca -ATPase antibodies have become available in recent years. Studies with these antibodies defined the localization of Ca " -ATPase in the sarcoplasmic reticulum of developing and mature skeletal muscles [60,262-270] and established a pattern of cross reactivity with various Ca -ATPase isoenzymes in the sarco(endo)plasmic reticulum [270-286] and in the plasma membrane [284,287-290] of skeletal, cardiac and smooth muscles. Antibodies have also proved useful in the quantitation of Ca -ATPase, both in muscles of diverse fiber types [291-294] and in COS-1 cells transfected with Ca -ATPase cDNA [97,103,126,127,129,215],... [Pg.88]

Kotlikoff I have a question about InsP3 receptors and ryanodine receptors. There is good evidence for wave propagation with both systems in smooth muscle. Can you say anything in experiments where you have looked with antibodies about the relationship between InsP3 receptors and ryanodine receptors And does this provide any insight into the interaction between these Ca2+-sensitive intracellular Ca2+ release channels ... [Pg.269]

Immunohistochemical analyses were performed using antibodies recognizing smooth muscle actin (SMA), troponin-T (Trop-T), troponin T-C (Trop T-C), myosin heavy chain (MHC), muscle actin (MA), a-actinin, a-SR-1, desmin, connexin-43, fibroblasts (all antibodies from Dako, Denmark). For fluorescent immunohistochemistry the AlexaFluor 594 goat anti mouse secondary antibody (Molecular Probes, Leiden, The Netherlands) was used. In addition, cell nuclei were stained using DAPI. [Pg.108]

Sheep anti-FITC-POD (Roche). Primary antibodies in this study we have used a mouse monoclonal antibody against smooth muscle a-actin (sm-a-actin, Dako) and rabbit polyclonal antibody against programmed cell death 4 (PDCD4, Rockland Immunochemicals). [Pg.356]

Like mast cell stabilizer, corticosteroids do not relax airway smooth muscle directly but reduce bronchial reactivity, increase airway caliber, suppress inflammatory response to antigen antibody reaction or trigger stimuli and reduce the frequency of asthma exacerbations. They produce more sustained symptomatic relief than any bronchodilator and mast cell stabilizer. [Pg.235]

Suppression of lymphocyte proliferation Suppression of antibody production by B lymphocytes Relaxes stomach and gallbladder smooth muscle H3Modulation of histamine synthesis and release Inhibits vagally mediated bronchoconstriction Vasodilatation... [Pg.240]

In response to the attachment of the antigen to the IgE antibodies, the macrophages release mediators such as histamine, which causes release of further mediators such as cytokines and leukotrienes. These inflammatory mediators cause the dilation and increased permeability of blood vessels and constriction of smooth muscles. [Pg.252]

The antibody fragment also binds to vitronectin receptors (av integrin) that are present on a number of tissues including vessel wall endothelial cells, smooth muscle cells and platelets. These receptors are involved in the proliferative properties of endothelial and smooth muscle cells and the procoagulant properties of the platelets. [Pg.115]

Fig. 6.1 Immediate hypersensitivity reaction. These reactions are the result of the production of IgE antibody in response to an allergen. IgE binds to the mast cells via Fc receptors and its reexposure to the allergen causes degranulation and secretion of endogenous mediators. In allergic responses, TH2 cells are important in recognizing allergens in the context of MHC molecules and secrete IL-4, IL-5 and IL-13. IL-4 induces isotope switching from IgG to IgE, and IL-5 is involved in eosinophil recruitment. IL-8 serves as a chemical signal to attract neutrophils at the site of inflammation. The collective effects of endogenous mediators include rashes, inflammation, smooth-muscle contraction, bronchospasm, asthma and severe anaphylactic shock, which may even cause death (see Color Insert)... Fig. 6.1 Immediate hypersensitivity reaction. These reactions are the result of the production of IgE antibody in response to an allergen. IgE binds to the mast cells via Fc receptors and its reexposure to the allergen causes degranulation and secretion of endogenous mediators. In allergic responses, TH2 cells are important in recognizing allergens in the context of MHC molecules and secrete IL-4, IL-5 and IL-13. IL-4 induces isotope switching from IgG to IgE, and IL-5 is involved in eosinophil recruitment. IL-8 serves as a chemical signal to attract neutrophils at the site of inflammation. The collective effects of endogenous mediators include rashes, inflammation, smooth-muscle contraction, bronchospasm, asthma and severe anaphylactic shock, which may even cause death (see Color Insert)...
Continuous intraperitoneal infusion of insulin causes increased insulin immunogenicity, but it is not known if this is accompanied by an increased frequency of autoimmune diseases. Antibodies against insulin, thyroglobulin, thyroperoxidase, gastric parietal cells, smooth muscle,... [Pg.402]


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See also in sourсe #XX -- [ Pg.117 , Pg.679 ]




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