Receptor on cell surfaces

Figure 48-3. Schematic representation of fibronectin. Seven functional domains of fibronectin are represented two different types of domain for heparin, cell-binding, and fibrin are shown. The domains are composed of various combinations of three structural motifs (I, II, and III), not depicted in the figure. Also not shown is the fact that fibronectin is a dimer joined by disulfide bridges near the carboxyl terminals of the monomers. The approximate location of the RGD sequence of fibronectin, which interacts with a variety of fibronectin integrin receptors on cell surfaces, is indicated by the arrow. (Redrawn after Yamada KM Adhesive recognition sequences.

Stump, R.F., Pfeiffer, J.R., Schneebeck, M.C., Seagrave, J.C., and Oliver, J.M. (1989) Mapping gold-labeled receptors on cell surfaces by backscattered electron imaging and digital image analysis Studies of the IgE receptor on mast cells. Am. J. Anat. 185, 128-141. 

F(ab )2 fragments of antibodies are generated by pepsin digestion of whole IgG antibodies to remove a portion of the Fc region (see Sect. 1.1). Elimination of nonspecific binding of the Fc region of antibodies to Fc receptors on cell surfaces in... 

Three TNF antagonists are currently approved for the treatment of RA etaner-cept (ETN), infliximab (INF), and adalimumab. ETN a fusion protein of two identical chains of the recombinant human TNF receptor, p75, fused with the Fc portion of human immunoglobulin (Ig) G1 binds to soluble TNF-a in vivo. INF and adalimumab are both monoclonal antibodies to TNF-a INF is chimeric, and adalimumab is fully humanized. Both bind to soluble TNF-a, preventing TNF-a from binding to its receptors on cell surfaces. INF can also bind transmembrane TNF-a, fix complement, and cause cell lysis. 

Adalimumab is a completely human IgGi approved for use in rheumatoid arthritis. Like the other anti-TNF- biologicals, adalimumab blocks the interaction of TNF- with TNF receptors on cell surfaces it does not bind TNF-3. Pharmacodynamic studies showed that administration of adalimumab reduced levels of C-reactive protein, erythrocyte sedimentation rate, serum IL-6, and matrix metalloproteinases MMP-1 and MMP-3. In vitro, adalimumab lyses cells expressing TNF- in the presence of complement. Patients may self-administer single doses of the antibody subcutaneously, every other week. Adalimumab has a serum half-life of 2 weeks, which is increased by 29-44% in patients who are also taking methotrexate. 

The protein moieties of lipoproteins are recognized by receptors on cell surfaces. In lipid uptake from the intestine, chylomicrons, which contain apolipoprotein C-II (apoC-ID, move from the intestinal mucosa into the lymphatic system, and then enter the blood, which carries them to muscle and adipose tissue (Fig. 17-1, step... 

Lipoproteins interact with enzymes (e.g., lecithin cholesterol acyltrans-ferase, or lipases), with lipid transfer proteins, or with receptors on cell surfaces. The composition of a lipoprotein class depends upon the results of these kinds of interactions. Ultracentrifugation itself may result in minor changes in lipoprotein composition (see Sections 6 and 6.1). 

In the congenital disease familial hypercholesterolemia, the high circulating level of cholesterol is due to the complete absence of LDL receptors or to the presence of defective receptors on cell surfaces. 

Important components of cell membranes, including receptors on cell surfaces that control the passage and/or action of various chemicals that influence the cell. 

Although it is not possible to delineate the mechanisms by which interferon beta-lb exerts its activity in MS. it is known that the interferon binds to specific receptors on cell surfaces and induces the expression of a number of interferon-induced gene products, such as 2. 5 -oligoadenylate synthetase and protein kinase. Additionally, interferon beta-lb blocks the synthesis of INF-y. which is believed to be involved in MS attacks. 

Etiology of Type II Hyperlipoproteinemia - In a study of the inheritance of xanthomatosis and hyper- -lipoproteinemia, the segregation pattern satisfied the criteria for autosomal dominant inheritance, but not for a polygenic trait. The genetic analysis demonstrated that hyperlipoproteinemia Type Ila and Type lib were the same disease.7 8 Defective removal of low density lipoproteins (LDL) from the circulation produced the elevated LDL and plasma cholesterol observed in Type II hyperlipoproteinemia. This defect appeared to be related to the decreased number of LDL receptors on cell surfaces (for reviews see 9, 10), although a change in the permeability of the cell membrane to cholesterol may also play a prominent role. 

Anabolic Agent, Hormone replacement. Selectively binds to GH receptors on cell surfaces and blocks binding of endogenous GH. 

After insulin binds to insulin receptor on cell surface, insulin receptor and its substrates are phosphorylated, which leads to activation of various insulin signaling pathways [202]. Reynoso et al. [203] evaluated several aspects of the insulin resistance induced by palmitic acid in rats and found that after treatment with 0.09 g/kg of palmitic acid there is a delay in the curve of tolerance to glucose. The authors concluded that occur an increase in the phosphorylations in serine of the insulin receptor after the treatment with palmitate, suggesting that PKC has a role as negative regulator of the insulin receptors activation in the insulin resistance induced by palmitic acid. 

The binding of large and small extracellular substances to receptors on cell surfaces, particularly the interactions with paramyxovirus and the functions of sialoglyco-proteins on erythrocyte membranes, has been reviewed. The roles of glycoproteins in the membranes of mitochondria, milk-fat globules, and lysosomes and the interactions of lectins associated with intracellular membranes have been discussed. ... 

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