Meaning of‘Site

On the basis of chemical modification studies, Tyr 198 of carboxypeptidase A was proposed to act as a proton donor (i.e., a general acid) in the mechanism of catalysis. However, when Tyr 198 was replaced with Phe by means of site-directed mutagenesis, the modified enzyme retained substantial enzymatic activity, indicating that the tyrosyl hydroxyl may not have a specific role in catalysis. 

It has been established, by means of site-directed mutagenesis experiments, that three amino acid residues are essential for the overall catalysis, namely the glycyl radical (Gly734) and two consecutive cysteines at positions 418 and 419. Two mechanisms were proposed for PFL at the time when the theoretical study was performed. Although based on the same experimental information, these two mechanisms are quite different (Figures 10 and 11). 

Phosphoenolpyruvate carboxylase (PEPC) of Thermus sp., was characterized and its mechanism of stabilization was studied by means of site-directed mutagenesis. A divergent sequence at a Gly-rich region of Thermus PEPC was revealed to contribute to the activity at hi temperature but not to the tolerance to the irreversible heat inactivation. 

Hagglund, B. and Lundmark, J.-E. (1977). Site index estimation by means of site properties. Scots pine and Norway spruce in Sweden. Stud. For. Suec. 138, 1-38. 

Fibril formation in human calcitonin (hCT) from aqueous solution at pH 4.1 was examined and compared with those at pH 3.3 and 7.5 by means of site-directed C solid state NMR. The observed chemical shifts and lineshapes of the CP MAS spectra differed substantially among fibrils prepared at different pHs. It was found that antiparallel P-sheet structures were formed at pH 7.5 and 4.1 in the central core regions. Further, an attempt was made to assess interatomic distances by REDOR measurements between amide nitrogen and carbonyl carbon of neighboring chains of C, N-labelled hCT. A unique chain packing of the antiparallel P-sheets was proposed as a dominant fibril structure. 

Lifetime excess risks, also referred to as lifetime attributable risks (Kellerer et al. 2001, BEIR VII 2006), LAR, are calculated by means of site-specific risk models, site-specific baseline rates on cancer incidence (or cancer mortality), and life-table data to account for competing risks ... 

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