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Proteins replacement

An examination of mutant PKA proteins was undertaken. Phosphorylation of Thr-197 is required to activate PKA and phosphorylation of Ser-338 enhances stability of the protein. Replacement of Thr-197 and/or Ser-338 by Ala was examined to determine any conformational changes in the protein. Both single substitution mutants were expressed in Escherichia coli in similar levels to wild-type protein. However, both mutants were found to be less stable, as had been previously described. The double mutant... [Pg.26]

Several techniques have now been developed for completely removing the iron from non-heme proteins, replacing the iron and reconstituting their chemical activity. The most effective method is to use the mercurial. [Pg.150]

Figure 8.5 Interaction potential for model whey protein layer consisting of densely packed brush-like tethered chains with small a fraction of the whev protein replaced by p-casein chains as represented by a copolymer model. The energy A d) calculated from SCF theory is plotted as a function of surface-surface separation d A, no p-casein B, 2.5% p-casein C, 5% p-casein D, 5% p-casein alone (without whey protein layer). Potentials A, B and D imply that the emulsion system is flocculated potential C implies a stable emulsion state. Reproduced from Dickinson (2006b) with permission. Figure 8.5 Interaction potential for model whey protein layer consisting of densely packed brush-like tethered chains with small a fraction of the whev protein replaced by p-casein chains as represented by a copolymer model. The energy A d) calculated from SCF theory is plotted as a function of surface-surface separation d A, no p-casein B, 2.5% p-casein C, 5% p-casein D, 5% p-casein alone (without whey protein layer). Potentials A, B and D imply that the emulsion system is flocculated potential C implies a stable emulsion state. Reproduced from Dickinson (2006b) with permission.
The fatty acid chains are evidently embedded in the outer membrane as an anchor. About one-third of the lipoprotein molecules are attached covalently to the peptidoglycan through an amide linkage between the side chain amino group of the C-terminal lysine of the protein and a diaminopimelic acid residue of the peptidoglycan (Fig. 8-29). Thus, the protein replaces one of the terminal D-alanine residues of about one in ten of the murein peptides. There are 2.5 x 105 molecules of the bound form of the lipoprotein per cell spread over a surface area of peptidoglycan of 3 pm2. They appear to be associated as trimers located primarily in the periplasmic space.589... [Pg.428]

The structure of the E. coli enzyme (Fig. 16-24) shows methylcobalamin bound in a base-off conformation, with histidine 759 of the protein replacing dimethylbenzimidazole in the distal coordination position on the cobalt. This histidine is part of a sequence Asp-X-His-X-X-Gly that is found not only in methionine synthase but also in methylmalonyl-CoA mutase, glutamate mutase, and 2-methyleneglutarate mutase. However, diol dehydratase lacks this sequence and binds adenosylcobalamin with the dimethylbenz-imidazole-cobalt bond intact.417... [Pg.875]

Since the mid 1960s, with the discovery of cryoprecipitate by Judith Graham Pool, there has been a growing understanding of the biology associated with protein replacement therapies (Pool and Shannon, 1965). A serious recurring obstacle to protein replacement therapies is the development of inhibitory antibodies in some... [Pg.69]

There are two protein replacement products available for A1AD, both pooled human plasma donor-derived products. Approval of these products was based upon replacement of serum AAT to the above-mentioned levels. Neither has been proven to prevent lung disease in a prospective, double-blinded placebo-controlled fashion, but retrospective registry data suggest a beneficial effect. However, protein replacement therapy has been very safe. Particularly remarkable has been the lack of an adaptive immune response by patients on therapy, which may relate to the genetic homogeneity of this A1AD population, in which approximately 95% have one particular missense mutant allele (PI Z). [Pg.86]

The rationale for gene therapy of A1AD is strongly supported by the safety and efficacy of the protein replacement. rAAV-produced AAT is efficiently secreted from a number of different... [Pg.86]

Prior to 1961, all the factors that catalyzed the photoreduction of pyridine nucleotides had been isolated from either chloroplasts or leaves. The green plant was considered the only source of these proteins. However, in 1961 the association of these proteins with green plants ceased to be unique when Losada, Whatley, and Arnon (64) isolated a similar protein from a photosynthetic bacterium. This bacterial protein replaced the chloroplast protein in the photoreduction of TPN by illuminated spinach chloroplast fragments. [Pg.111]

Animal origin products such as eggs, milk, fish, red meats and poultry contain low amounts of manganese. Absorption of such minerals as iron, copper, phosphorus and calcium is superior from animals products than from plant-origin foods. As reported by Kies et al. (in this book), manganese apparently is better absorbed by humans from meals containing meat and fish than from those containing plant-protein replacement products. Because of the low content... [Pg.4]

The vanadium nitrogenase has been isolated from A. vinelandii and A. chroococcum (Table 1). With the molybdenum in the protein replaced by vanadium, the vanadium nitrogenase resembles its molybdenum counterpart. It has the molybdenum-iron (MoFe) protein equivalent in the vanadium-iron (VFe) protein, as well as the iron (Fe) protein equivalent. [Pg.3116]

In 1981, the pheromone binding protein (PBP) and sensilla esterase (SE) of Antheraea polyphemus were identified [44] and in 1985 a new model for pheromone detection was proposed, in opposition to the previous model. In this model, PBPs transported pheromone to receptor proteins (replacing pore-tubules in this role) and SE rapidly inactivated pheromone by enzymatic degradation [45]. PBPs have become established as only a subclass of a much larger family of insect OBPs that are represented at least throughout the neopterous insects, from cockroach to honeybee. [Pg.398]

Gene therapy may be defined as the administration of exogenous DNA, in the form of intact gene(s) for therapeutic purposes. There are some a priori characteristics for diseases that are likely to be attractive targets for gene therapy, and a fundamental contrast between the gene therapy of protein replacement, in comparison with protein synthesis regulation. [Pg.286]


See other pages where Proteins replacement is mentioned: [Pg.235]    [Pg.107]    [Pg.843]    [Pg.866]    [Pg.65]    [Pg.65]    [Pg.158]    [Pg.38]    [Pg.333]    [Pg.414]    [Pg.61]    [Pg.11]    [Pg.825]    [Pg.299]    [Pg.107]    [Pg.136]    [Pg.58]    [Pg.70]    [Pg.210]    [Pg.10]    [Pg.41]    [Pg.789]    [Pg.80]    [Pg.235]    [Pg.106]    [Pg.198]    [Pg.217]    [Pg.235]    [Pg.825]    [Pg.587]    [Pg.813]    [Pg.32]    [Pg.222]    [Pg.429]   
See also in sourсe #XX -- [ Pg.466 ]

See also in sourсe #XX -- [ Pg.32 ]




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Protein crystallography isomorphous replacement

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Protein replacement therapy

Protein-based fat-replacer

Proteins selenomethionine replacement

Replacement modifications proteins

Replacing Missing Proteins

Water replacement hypothesis, protein

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