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Cell surface alterations

Neoantigens Ectopic hormones Enzyme abnormalities Increased proliferation Altered differentiation Endothelial-stimulating factors Invasion Metastasis Neoantigens Ectopic hormones Enzyme abnormalities Altered cell surface Altered cytoskeleton Chromosome abnormalities... [Pg.187]

Indicators De-differentiated Uncontrolled cell division Altered cell surface Altered cytoskeleton and nucleus... [Pg.401]

Karasaki, S., 1976, Ultrastructural and cytochemical studies on hyperbasophilic foci with special reference to the demonstration of cell surface alterations in hepatocarcinogenesis. Cancer Res. 36 2567. [Pg.148]

Cell surface alterations Formaldehyde Outer membrane proteins appear to be involved... [Pg.192]

Vadyvaloo, V., Arous, S., Gravesen, A., et al. (2004). Cell-surface alterations in class 11a bacteriodn-resistant Listeria manacytagenes strains. Micrabialagy 150, 3025—3033. [Pg.99]

Several factors can influence metal uptake by stream autotrophic biofllms in fluvial systems. These include chemical factors (pH, saUnity, phosphate concentration) which affect metal bioavailabiHty by either altering the speciation of the metal or by complexing it at the biotilm s matrix and cell surfaces [18, 40], and also other biological and physical factors. [Pg.46]

The same ceUs that secrete collagen also secrete fi-bronectin, a large glycoprotein present on cell surfaces, in the extracellular matrix, and in blood (see below). Fi-bronectin binds to aggregating precollagen fibers and alters the kinetics of fiber formation in the pericellular matrix. Associated with fibronectin and procollagen in... [Pg.537]

HFE has been shown to be located in cells in the crypts of the small intestine, the site of iron absorption. There is evidence that it associates with P2 niicroglobu-lin, an association that may be necessary for its stability, intracellular processing, and cell surface expression. The complex interacts with the transferrin receptor (TfR) how this leads to excessive storage of iron when HFE is altered by mutation is under close smdy. The mouse homolog of HFE has been knocked out, resulting in a potentially useful animal model of hemochromatosis. [Pg.587]

It is suggested that altered cells which could be potentially malignant are recognized by the immune system and eliminated. This must mean that cancer cells possess new antigens on their cell surface. These antigens have been identified and can be categorized into three groups. [Pg.301]

The hydrophilic gold(I) drugs which need to be injected such as AuSTm and AuSTg, cannot easily move into most cells. Instead, they bind to cell surfaces where they can alter membrane transport and affect the overall cell metabolism [115, 134]. [Pg.305]

Flanagan, J. G and Leder, P. (1990). The kit ligand a cell surface molecule altered in Steel mutant fibroblasts. Cell 63 185-194. [Pg.39]

Different metal species vary in their biological reactivity.98 99 For example, the free ionic form of a metal may act by substituting a cofactor for a vital enzyme. Hydroxylated metal ions have been suggested to bind to the cell surface and alter the net charge of the cell to reduce its viability.101 Because different species may have different effects on biological processes, some species may be more toxic than others. There is a paucity of information in the literature regarding the relative toxicity of different metal species. [Pg.417]

The binding of a hormone to its receptor initiates intracellular events that direct the hormone s action. Ultimately, all hormones produce their effects by altering intracellular protein activity. However, the mechanism by which this occurs depends on the location of the hormone receptor. Receptors are typically located on the cell surface or in the cell nucleus. As a result, most hormones carry out their effects by means of two general mechanisms ... [Pg.116]

Figure 10.1 ThecyclicAMPsecondmessengersystem.Themostcommonsecond messenger system activated by the protein/peptide hormones and the catecholamines involves the formation of cAMP. This multistep process is initiated by binding of the hormone (the first messenger) to its receptor on the cell surface. The subsequent increase in the formation of cAMP (the second messenger) leads to the alteration of enzyme activity within the cell. A change in the activity of these enzymes alters cellular metabolism. Figure 10.1 ThecyclicAMPsecondmessengersystem.Themostcommonsecond messenger system activated by the protein/peptide hormones and the catecholamines involves the formation of cAMP. This multistep process is initiated by binding of the hormone (the first messenger) to its receptor on the cell surface. The subsequent increase in the formation of cAMP (the second messenger) leads to the alteration of enzyme activity within the cell. A change in the activity of these enzymes alters cellular metabolism.
Attachment There is a high specificity in the interaction between virus and host. The most common basis for host specificity involves the attachment process. The virus particle itself has one or more proteins on the outside which interact with specific cell surface components called receptors. The receptors on the cell surface are normal surface components of the host, such as proteins, polysaccharides, or lipoprotein-polysaccharide complexes, to which the virus particle attaches. In the absence of the receptor site, the virus cannot adsorb, and hence cannot infect. If the receptor site is altered, the host may become resistant to virus infection. However, mutants of the virus can also arise which are able to adsorb to resistant hosts. [Pg.124]

The number of channels synthesized, processed, and trafficked to the apical membrane and rate of CFTR internalization at the apical membrane determine the cell surface density. Mutations in CFTR that alter one or more of these parameters decrease total CFTR-mediated anion flux and impair epithelial cell function. [Pg.159]


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See also in sourсe #XX -- [ Pg.192 ]




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