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Our mutant work suggests that variation in synthetic auxin sensitivity is regulated by two components.
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The reduced light reflectivity in the TM23 mutant found in this work suggests a reduced density of cellular ultrastructure content.
Although our collection of expression microarrays do not include any records in which NFI-1 mutants were probed for genome-wide expression, previous work suggests that NFI-1 is critical for wild-type adult lifespan (Lazakovitch et al. 2005).
Therefore, our work suggests that atorvastatin can overcome gefitinib resistance in KRAS mutant NSCLC cells irrespective of the PTEN and PIK3CA statuses.
Most impartial work suggests they are wrong.
The new work suggests that it is.
Recent work suggests that the origin of both the fitness reduction conferred by the H275Y mutation and the unique fitness of the A/Brisbane/59/2007 mutant strain is found in the virus NA activity and surface expression.
Our work suggests that this movement and 'fill in' is, at least in part, performed by the ISWI family of remodelers, as we have demonstrated a reduction of the 'fill in' in the rsc isw1 double mutant.
Should cell death induction by the VE analog MitoVES be dependent on its binding to the Qp site of CII as our previous work suggested, then the efficacy of this agent would be compromised in Qp site mutants.
Our previous work suggested that srn exhibited a neurogenic phenotype, specifically an increased number of primary motor neurons [16], similar to that observed in mutants in the Notch-Delta pathway.
The OTULIN N341D mutant worked best with Met1-diUb E16Qprox, suggesting that the requirement for a negative charge was partially compensated.
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