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Male mutants from this line were bred to females of different genetic background including 129S1, FVB inbred lines and CF1 outbred mice.
We assessed both the original network (steps = 0) and a sample of 1-, 2-, and 3-step mutants from this network.
In order to investigate the role and function of the glycan shield of the viral envelope, we previously developed a panel of deglycosylated mutants from this pathogenic SIVmac239 backbone [2].
Selection of barium and amantadine-resistant mutants from this procedure uncovered a mutant, Kcv_Back, that was found to bear a single change, T63S, that was responsible for both phenotypes (Figure 2A and B).
We have decided to remove all observations on preimplantation G9a mutants from this manuscript.
Putative mutants from this screen were designated tgr for t rans g ene r eactivated.
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By following this protocol, 335 Sav mutants from the targeted 336 Sav mutants are obtained.
The first mutant from this screen to be described in detail has a defect in LTA4 hydrolase, an enzyme that is responsible for the production of proinflammatory leukotrienes.
Although the best mutant from this first round, designated Tx-Xyn-AF7, displays a wild-type amino acid sequence, its DNA sequence contains two mutations (at nucleotide positions 27 and 516) that cause approximately twofold higher expression of the recombinant enzyme.
To elucidate this phenomenon, studies were conducted using deletion mutants from the AOX2 promoter region.
Mutants from the X-Men comic book.
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