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Due to poor expression and stability of the Tob W93A mutant, we were unable to test the interaction of this mutant with CNOT7 in vitro, although the mutant expressed in mammalian cells for subsequent interaction assays in vivo.

By combining this strain with a previously engineered xylose reductase mutant, we were able to eliminate l-arabinitol formation and produce xylitol to near 100% purity from an equiweight mixture of d-xylose, l-arabinose, and d-glucose.

Since lysine762 localizes to the region that is deleted in the Δ716 G-CSFR mutant, we were interested in investigating whether cells expressing the K762R/G-CSFR also exhibited ligand-induced hyperproliferative responses to G-CSF.

In addition, by generating a MSMEG∆ furB mutant, we were able to show that FurB is involved in mptABC regulation.

Taking advantage of the growth defect at 37° of eso1-G799D mutant, we were able to screen for suppressors of the temperature sensitive phenotype by growing the double mutants at 25° and 37°.

By packaging the viral vector with the inactive D64V integrase mutant we were able to increase the amount of circular substrates 4-fold and at the same time abolish the viral integration machinery.

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This information is crucial for the analysis of a mouse model for cystinosis which, in the absence of a spontaneous mouse mutant, we are currently generating in order to study the pathogenesis of cystinosis in vivo.

Despite numerous attempts to generate Δpv1 mutants, we were unable to isolate such parasites, although control experiments were successful.

By combining gene expression analyses using 70-mer oligonucleotide 16.4 K microarrays for both wild type symbionts and nodulation defective symbiotic mutants, we were able to identify and classify more than 3,400 differentially regulated genes and associated regulators.

For some mutants, we were able to identify a region in which the mutation could be localized by deficiency mapping.

With these two new mutants we were able to show a significant impact on GAG-binding affinity.

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