Sentence examples for Major mutants from inspiring English sources

We begin to address the physiological targets of the Leishmania ISPs by creating L. major mutants deficient in ISP2 and ISP3 and characterizing their phenotype during the early phases of macrophage infection.

Introduction of second site mutations that disrupt a diarginine (RXR -based ERXR -basedn motif in thERfiretentionotide binding domotifrescues the traffinking defecthefirsttaF508-CFTR, supportinucleotidefor these motifs in mediating ER retention of the major mutant.

The major mutant point was at amino acid R882 and has a significantly poorer outcome [ 37].

In this study we created an L. major mutant deficient in all three ISP proteins (Δ isp1/2/3).

An L. major mutant deficient in all three ISP genes (Δ isp1/2/3) was generated and compared with Δ isp2/3 mutants to elucidate the physiological role of ISP1.

In previous studies of the Spanish population, the p.Arg1129Leu variant was identified as a major mutant allele which accounted for 24% of the STGD alleles.

Although the T6ES3ES4E L. major mutant protein mislocalized to the cytosol, P-orthophosphate labelling revealed no detectable radiolabelled HASPB while the triple mutation led to disruption of the N-myristoylation site (Fig. 2), reflecting the divergence in the enzyme recognition site between Leishmania and mammalian cells.

Confocal microscopy, SIEM and TIEM were also carried out on late passage wild-type parasites, together with L. major mutant lines either deleted for or complemented with the LmcDNA16 locus encoding the HASP and SHERP genes (McKean et al., 2001; Sadlova et al., 2010); these are the cDNA16 KO and Kin lines respectively (as described in Table S1B).

Mutants (C26A+G54A) and (U25A+C26A+G54A+U281A) were also identified as major adaptive mutants in the natural HpSVd-grapevine and HpSVd-hop isolates during persistent infection in hops.

In InI treatment naive patients polymorphic integrase sequence variation was common, with no major resistance mutants.

The discovery of the "gain of function" property of the CD-associated major NOD2 mutants challenges the paradigm about how human gene mutations cause diseases, and inspires the designing of novel therapeutic strategies for the treatment of CD and certain genetic disorders.