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Of 12 laboratory studies, 4 reported this interaction and 8 did not.
We observed a stronger positive association between NO2 and BP in participants with CVD, similar to Sørensen et al. (2012), who reported this interaction between long-term residential NOx and DBP.
In the Kin3-Mg-ADP reconstruction, helix-α6 contacts α-tubulin as was previously reported; this interaction is likely to involve basic residues conserved in Kin3 (discussed below) and negatively charged residues in the N-terminal region of α-tubulin H12.
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The Langmuir model assumes that both binding partners are homogenous, the analyte is monovalent, and that all binding events are independent [27].This analysis indicates a KD of 570±30 nM and the observed Bmax value is consistent with a 1∶1 binding stoichiometry; these binding characteristics, in the presence of 150 mM NaCl, are in agreement with ones previously reported for this interaction [28].
In this context, it should be noted that conflicting results have been reported on this interaction, which may be related to experimental and cell specific differences [ 11, 14].
However, the current TKA study was not in accordance with [ 46] which reported that this interaction enhanced the cell wall inhibitory action of vancomycin, but rather our finding suggested this interaction could adversely affect therapeutic outcomes.
This is not uncommon, as strong co-immunoprecipitation of the insulin receptor and IRS1 in a yeast two-hybrid system has also been reported, but this interaction is very difficult to observe in human skeletal muscle (L. J. Mandarino, unpublished results) [ 33].
Although several studies have reported the interaction between this endophyte and host plants for growth promotion, most studies have reported in vitro data [ 22, 27, 28, 36].
Their finding that the three Rho GDIs 1, 2 and 3 can all interact with RhoH is a matter of controversy, as others report that this interaction was only marginally detectable [ 61].
In this paper, a new strategy for studying protein interactions is reported; this method is based on the use of protein-imprinted polymers (PIPs).
We report that this interaction between MCs and tumor cells is an underlying mechanism for facilitating metastasis in the arthritic mice.
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