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To understand the altered transcriptional regulatory mechanism of this mutant, we aimed to establish possible relationships between gene expression and cis-regulatory information content.
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By studying these mutants, we aim to infer structural features of Aβ and its function in membranes.
To study how dauer remodeling is initiated, we aimed to identify mutants defective in this process.
In order to address the function of PGRP-SB1 in vivo, we aimed to generate a null mutant by homologous recombination.
Next, we aimed at generating DNA polymerase mutants with enhanced discrimination.
In this work, we aimed at identifying the signaling pathways associated to mutant MLK3, in particular the P252H mutation.
In the present work we aimed at exploring the impact of C2238/ αANP (mutant form) on atherosclerosis-related pathways.
In the current mutagenesis experiments we aimed to use the large number of point mutants to separate genetically the complementing movement and replication functions.
In the next series of experiments, we aimed to use and validate BLI to identify biofilm-defective mutants.
We aimed to identify the signal responsible for the observed increased growth of RGC arbors in kif5aa mutant tecta.
We aimed to study potential effect modification.
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CEO of Professional Science Editing for Scientists @ prosciediting.com