Heterologous interactions

Self-assembled monolayers (SAMs) [8] The layers are formed by heterologous interaction between reactive groups, such as thiols, and noble metals, such as gold or silver. Since the molecules are selectively adsorbed on these metals, film growth stops after the first monolayer is completed. The molecular aggregation is enthalpy driven, and the final structure is in thermodynamic equilibrium. 

A ring formed using exclusively heterologous interactions possesses cyclic symmetry. The trimer in Eq. 7-25 has a threefold axis Each subunit can be superimposed on the next by rotation through 360°/ 3. The oligomer is said to have C3 symmetry. Many real proteins, including all of those with 3,5, or another uneven number of identical protomers, appear to be formed of subunits arranged with cyclic symmetry. 

Now consider the quantitative aspects of heterologous interactions with ring formation. Let Kf be the formation constant and AG° the Gibbs energy change for the reaction of the / end of protomer P with the a end of a second protomer to form the dimer P2 (Eq. 7-25). 

Some enzymes, such as yeast hexokinase and creatine kinase (Chapter 12), associate in extremely asymmetric ways.102 A dimer is formed by means of heterologous interactions but steric hindrance prevents the unsatisfied sets of interacting groups from joining with additional monomers to form higher polymers. 

Heterologous bonding interaction 333, 334 Heterologous interactions 342 Heterologous square 352s Heteropolysaccharide(s)... 

Figure 9.11. Heterologous interactions between subunits in a trimer.

In contrast to the situation with the alternative nitrogenases, but with the notable exception of the C. pasteurianum proteins, the component proteins from aU. Mo-based nitrogenases interact as heterologous crosses to form catalyticaHy active enzymes (52). Carbon monoxide, CO, is a potent inhibitor of aU. nitrogenase-cataly2ed substrate reductions, with the exception of reduction (126). Molecular hydrogen has a unique involvement with Mo-nitrogenase... 

In this chapter, we review the interactions at the level of protein function, between opioid receptors and chemokine receptors, using both in vitro and in vivo model systems. As a part of this discussion, we also describe our current understanding of the biochemical pathway(s) that are involved in the heterologous desensitization process between these groups of receptors. 

Heterologous desensitisation refers to the desensitisation of the response to one agonist by the application of a different agonist. For example, desensitisation of a response to adrenaline by application of 5-HT is mediated by protein kinase A or protein kinase C because these kinases can phosphorylate receptors which are not occupied by agonist. Phosphorylation disrupts the receptor-G-protein interaction and induces the binding of specific proteins, arrestins which enhance receptors internalisation via clathrin-coated pits. Thus desensitisation of G-protein-coupled receptors results in a decrease in the number of functional receptors on the cell surface. 

The complementation experiments in which the A domain of a class 111 E-II is used as the phosphoryl group donor to the B domain of a second E-II molecule with either the same or different sugar specificity, while both are fixed in a membrane matrix, raises some intriguing issues about the association state of these proteins and the kinetics of their interactions. Do E-IIs form stable homologous complexes in the membranes If so, is it necessary to postulate the formation of stable heterologous complexes to explain, for example, the phosphorylation of the B domain of E. coli 11° by the A domain of ll , or can the data be explained by assuming a... 

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