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If calpain cleavage at this site is involved in the degradation of mHDx-1, VL12.3 binding would be expected to reduce turnover.
Protein subsets that form highly stable structures within the complex, by, for example, covalent binding, would be expected to act as a single protein with a common FR value.
Thus, VL12.3 binding would be expected to interfere with cleavage at AA 15 and possibly sterically hinder cleavage at AA 8. To determine the effect of compromising cleavage at AA 15 on mHDx-1 clearance, we performed a TR-FRET assay to measure soluble mHDx-1 levels in lysates of organotypic brain slice cultures biolistically transfected with mHDx-1 alone or with either VL12.3 or CVL, a control iAb.
Thus, the time taken for recovery is related to protein affinity, and an inhibitor of protein binding would be expected to reduce recovery time [ 16].
Thus variants with reduced heme binding would be expected to alter PLP binding and yield a protein with reduced function, as was observed for these two alleles.
If T286 phosphorylation would induce the most effective CaMKII binding to GluN2B (as stated), binding would be expected to be more extensive after LTD compared to LTP.
Similar(53)
Therefore, zinc finger motifs offer an attractive framework for the design of novel DNA binding proteins, and such a DNA binding protein would be expected to possess a unique binding sequence with high specificity and affinity.
DNA binding was dependent on the size of the DNA fragments used in the assay, suggesting there were multiple sites for binding, as would be expected of a protein binding to DNA in a sequence-independent manner.
These results indicate that the ability of arrestin to trap retinal in the rhodopsin "hydrophobic patch" mutant L226A was impaired (presumably because of impaired arrestin binding), as would be expected if arrestin employs part of the same interaction mechanism for binding to rhodopsin as the Gtα C-terminal tail does.
If DNA binding were necessary for PARP-dependent mADPR accumulation, the PARP-dZF1 mutant, which has little or no detectable DNA binding capacity, would be expected to show little or no ability to reconstitute O/N stress-induced NAD degradation or TRPM2 activation in the DT40 system.
Given that epibatidine shows large functional potency differences at α4 β2 vs. α4 α4 interfaces, biphasic binding properties would be expected at (α4 3 β2)2 receptors.
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