phage display selection of engrailed homeodomain

Abstract not found

on the Tanford-Kirkwood and Poisson-Boltzmann models. The NMR data reveal that the global conformation of wild-type R-sarcin is preserved in the H50Q, E96Q, H137Q, and H50/137Q variants, and that His137 is involved in an H-bond that is crucial in maintaining the active site structure and in reinforcing

, and Mono-Q column chromatography. Epoxy-activated Sepharose 6B affinity chromatography was used for large-scale purification. The presence of OP and CB pesticide residues in agricultural samples was assayed on the basis of AchE inhibition value. The presence (6 bands) or absence of some colored bands

observations of effective Q argue that the high velocity anomaly is in the upper mantle. A model that satisfies the observed residual differences and which is consistent with additional seismic data possesses an anomalous zone which begins beneath the MohoroviEiC discontinuity, at a depth of 40-50 km, extends

to monomethylated arsenicals (MMA) when M103A, Q107A and I136A were used as the enzyme. The Vmax (the maximal velocity of the reaction) values of M103A, Q107A, I136A and E137A were decreased to 8%, 22%, 15 % and 50 % of that of WT-hAS3MT, respectively. The KM(SAM) (the Michaelis constant for SAM) values of mutants

-shifted the glycine EC50 but did not affect ethanol sensitivity. It is noteworthy that the uncharged glutamine at position 52 (A52Q) caused only a small right shift of the glycine EC50 while increasing ethanol sensitiv-ity as much as A52E. In contrast, the shorter uncharged aspar-agine (A52N) caused the greatest

The clinical value of serial minimal residual disease (MRD) monitoring in core binding factor (CBF) AML by RT-qPCR was prospectively assessed in 278 patients (163 with t(8;21) and 115 with inv (16)) entered in the UK MRC AML 15 Trial. CBF transcripts were normalised to 105 ABL copies. At remission

The authors simulate climate change for 1951–2050 using the GISS SI2000 atmospheric model coupled to HYCOM, a quasi-isopycnal ocean model (‘‘ocean E’’), and contrast the results with those obtained using the same atmosphere coupled to a passive Q-flux ocean model (‘‘ocean B’’) and the same

derivatives of benzene and toluene, DNA shuffling of the alpha-hydroxylase fragment of ToMO (TouA) and saturation mu-tagenesis of the TouA active site residues I100, Q141, T201, and F205 were used to generate random mutants. The mutants were initially identified by screening with a rapid agar plate assay