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It would be interesting to determine whether this modification is also involved in the Che-1/p53 interaction.
Oligomers of glutathionylated apo-SOD1 were also probed with C4F6 to determine whether this modification induces structural rearrangements that enhance exposure of the disease-specific epitope.
While H4 lysine 5 acetylation clearly correlated with malignant phenotype of the breast cancer cell lines, it will be important to determine whether this modification plays a causative role.
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We initially performed our top-down MS studies on histone H2B, as this histone has more recently been shown to be monomethylated at lysine 5 in humans [41], [42], and we were interested in determining whether this modification is conserved or if alternative sites of methylation exist in budding yeast.
To determine whether the modification of culture conditions can stimulate cell proliferation, hUCB-MSCs were treated with Ca2+, hypoxia, or combined Ca2+/hypoxia.
These were picked and backcrossed to the parental Dystrophin mutant females to determine whether the modification was on the second or third chromosomes.
To determine whether the modification of histone turnover in and of itself could lead to the modulation of the chromatin state, we determined whether a known modifier of histone turnover (i.e., Mst2 [ 51]) could also influence heterochromatin propagation across the IR-L and matK loci of the ddb1Δ mutant.
The purpose of the present study was to examine the effects of ethanol on the phosphorylation of the ASGP-R to determine whether this post-translational modification could contribute mechanistically to the observed ethanol-induced alterations.
However, our data do not determine whether this occurs through modification of BMP4 signaling.
Further experimentation must be done to determine whether these modifications of GEFs also lead to regulation of Rac activity.
Therefore, we decided to determine whether these modifications were correctly incorporated in Bug22 axonemes.
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