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The present study was designed to investigate the role of plant mitochondria in redox sensing and hypersensitive response in a Nicotiana sylvestris mitochondrial mutant (CMSII mutant) that lacks a functional respiratory complex I.
Further, we constructed a soluble variant of the neurotoxic PrPΔCD mutant that lacks its glycosyl phosphatidyl inositol (GPI) membrane anchor.
A G2A Gag mutant that lacks myristoylation and fails to bind to membranes for assembly was used as a reference for a budding deficient Gag [2].
Accordingly, the p271 170 mutant that lacks both T198 and T187 resulted even more stable in the same assay (Figure 2B).
A mmaA4 knockout mutant that lacks keto- and methoxy-mycolates, showed reduced cell wall permeability and was also attenuated in mice [11].
The phyB-GFP or phyB-YFP fusion proteins are biologically active photoreceptors as their expression resulted in complementing the phyB-9 mutant that lacks detectable amount of the phyB photoreceptor [14].
ROS-induced cell death was suppressed by co-transfection of a FOXO3a mutant that lacks the activation-domain of transcription, transactivation of pro-apoptotic genes by FOXO was necessary to cause ROS-induced apoptosis [45].
In contrast with this observation several lines of evidence demonstrated that the p271 170 mutant (that lacks both the T198 and the T187 residues) has an expression comparable to that of the WT protein (Figures 1B, 2B, S1) and references [19], [21].
The role of the N-terminal domain was further probed by studying the nuclear transport of a Foxp3 mutant that lacks the N-terminal 51-aa, Domain 1 and lacks a functional Domain 2. The results show this mutant protein missing Domains 1, 2, and 3 is found almost exclusively in the cytoplasm (Fig. 6B, lanes 7 and 8).
Accordingly, a gc-null mutant that lacks both gca and sgc genes that together encode for all guanylyl cyclase activity extends ∼3 times more de novo pseudopodia; at the observed unaltered frequency of pseudopod splitting this leads to a strong reduction of the average length of the series of split pseudopodia from a = 6 in wild type to a = 2.5 in gc-null cells.
We found that an LXR L439A/E441A mutant that lacks co-activator recruitment capacity was unable to repress inflammation.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com