Cellular interaction with patterned

In 2D cell culture on chip, cell adhesion has been extensively studied on patterned surfaces for it is critical to cellular functions. Micropattems have been used to study the cellular interactions with various materials such as metals, polymers, self-assembled monolayers, extracellular matrix proteins, cell adhesion peptides, and other bioactive molecules. The physical and chemical properties of a substrate affect the attachment and growth of cells on it, and many studies have demonstrated that different topographical features of a surface affect cell attachment. Glass, sflicon, and polydimethylsiloxane (PDMS) are widely used as substrate materials of ceU culture microchips. 

The identification of the fold is, however, only a minor part of protein characterization. Function is a loosely defined term, but must be viewed within a particular context, e.g., protein function can only take place with an interaction partner or within cellular cascades and networks. Fold predictions and homology searches can only give partial answers to such higher order functions. Thus, independent functional features have to be collected and put into context. Such features include not only molecular properties, but also cellular roles, expression patterns, dysfunctions, pathway context, and subcellular localization. The latter can be predicted by exploiting a variety of methods and localization sites. Kenta Nakai reviews many such sites and their implementation... 

Clearly, further studies will be necessary to sort out the multiple factors involved in the in vivo immune response to C. neoformans carbohydrate-mimetic peptides. Several conclusions may be drawn from the results to date. Peptides that mimic the cryptococcal capsular polysaccharide show specificity, in that each peptide binds with differing affinity to closely related mAbs [140,149]. The pattern of binding to protective and nonprotective mAbs differs between the mimetic peptides and the polysaccharide [140]. Protective efficacy is related to the location of carbohydrate epitopes recognized by these mAbs, within the polysaccharide capsule, but hkely also depends on interactions between mAbs and cellular responses [149]. Peptides have been shown to be functional, immunogenic mimics, but their protective efficacy depends on multiple factors, including the type of Abs elicited and interactions with the cellular immune system. Protective efficacy does not correlate with binding affinity to representative mAbs, but rather depends on the nature of these interactions. 

Vincristine resistance has been studied in Chinese hamster ovary cell lines cells resistant to vincristine also are resistant to vinblastine and vindesine. Suggestions were made that, in cells with relatively low levels of drug resistance, at least two prominent mechanisms of resistance can occur (22). In the first instance, cellular resistance may be attributable to membrane alterations that are reversible, functionally, by treatment with verapamil. In the second, resistance has been postulated to be due to an altered sensitivity of tubulin to the effects of the drugs the primary basis for postulating an altered interaction with tubulin was that a subgroup of cells resistant to vincristine showed enhanced sensitivity to taxol, a drug that can stabilize microtubules. It should be emphasized that differential sensitivities of tubulins from different tumor cells to the effects of vincristine or vinblastine has been proposed as a basis for the susceptibilities of cells to the cytotoxic effects of such drugs (23). Differences have been described in the electrophoretic patterns for tubulins obtained from vin-... 

Although taxanes bind to p-tubulin promoting microtubule polymerization and stabilization of the spindle complex, they serve to cause a sustained mitotic block at the metaphase/anaphase boundary. This block will occur at a lower concentration than that which is required to increase the microtubule mass (10). However, it is not completely clear how this interaction with microtubules translates into cell death. Morphologic features and the characteristic DNA fragmentation patterns seen in the setting of apoptosis have been documented in tumor cells after therapy with taxanes (10). These observations are accompanied by the phosphorylation of Bcl-2, an anti-apoptotic protein, changing the cellular balance between Bax and Bcl-2 to a status that favors apoptosis (11). 

Protein function can be described on three levels. Phenotypic function describes the effects of a protein on the entire organism. For example, the loss of the protein may lead to slower growth of the organism, an altered development pattern, or even death. Cellular function is a description of the network of interactions engaged in by a protein at the cellular level. Interactions with other proteins in the cell can help define the lands of metabolic processes in which the protein participates. Finally, molecular function refers to the precise biochemical activity of a protein, including details such as the reactions an enzyme catalyzes or the ligands a receptor binds. 

Connection between Transport Processes and Solid Microstructure. The formation of cellular and dendritic patterns in the microstructure of binary crystals grown by directional solidification results from interactions of the temperature and concentration fields with the shape of the melt-crystal interface. Tiller et al. (21) first described the mechanism for constitutional supercooling or the microscale instability of a planar melt-crystal interface toward the formation of cells and dendrites. They described a simple system with a constant-temperature gradient G (in Kelvins per centimeter) and a melt that moves only to account for the solidification rate Vg. If the bulk composition of solute is c0 and the solidification is at steady state, then the exponential diffusion layer forms in front of the interface. The elevated concentration (assuming k < 1) in this layer corresponds to the melt that solidifies at a lower temperature, which is given by the phase diagram (Figure 5) as... 

The FGF family consists of 23 proteins that are classified by their expression pattern, receptor-binding preference, and protein sequence (20,21). FGF is present in the normal myocardium (22). Its expression is stimulated by hypoxia (23) and hemodynamic stress (24). FGF-2 is a pluripotent molecule and modulates numerous cellular functions for multiple cell types. In the context of angiogenesis, it induces endothelial cell proliferation, survival, and differentiation, and is also involved in cell migration of endothelial cells, smooth muscle cells, macrophages, and fibroblasts (21). These effects are mediated through its interaction with the tyrosine kinase receptor FGFRI which also leads to the downstream release of NO (25). Additionally, FGF-2 stimulates endothelial cells to produce a... 

Initiators interact with host cellular macromolecules and nucleic acids in specific patterns. The majority of known initiators have both initiating and promoting (see below) activity and can thus induce neoplasms rapidly and in high yield when there is repeated or high-level exposure. When given at sufficiently low single doses, an initiated cell requires subsequent promotion for the development of any neoplasia. Thus, the dose of an initiator is a critical determinant of its carcinogenic potential. 

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