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With the structural and biochemical data presented here, it is now clear that CupB2 is an FGS-type chaperone with two functionally different Ig domains.
The structure of NPC1L1 NTD) and the biochemical data presented here are consistent with in vitro cell culture assays demonstrating a high degree of specificity for cholesterol over other sterols.
The combination of genetic and biochemical data presented here strongly validates our comparative genomic derived predictions solving the long-standing mystery of 6-HMDP biosynthesis in most Archaea.
Our immunocytochemical and biochemical data presented here illustrate that ubiquitin and MAFbx/atrogin-1 protein expression and 20S proteasome activity were elevated in response to sustained moderate compression.
In isolation, these data could suggest that galactose exposure causes higher oxidative stress in mutants than in controls, but combined with the biochemical data presented here, the results suggest that there are differences in how the animals respond to oxidative stress rather than in the level of stress itself.
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Biochemical, ultrastructural and genetic data presented here demonstrate that gelsolin is a member of the whirlin complex and plays a role in stereocilia elongation.
The transcriptomics and proteomics data presented here, together with the biochemical characterization of DPSL place this ferritin-like protein cage at the center of a cellular oxidative stress scheme (Figure 9).
Overall, the NMR data presented here are in agreement with previous biochemical studies, further supporting the value of using stem-loop domains to improve our understanding of substrate activation and recognition within the context of the full ribozyme.
In summary, although impairment in intercellular glucose transport through GJs does not necessarily rule out the K+ recycling theory entirely, available data and the new data presented here seem to favor that effects of Cx30 null mutation on biochemical coupling are the major cause for hearing loss observed in these mutant mice.
The data presented here indicate that human mt-leucyl tRNA synthetase (LARS2) has the ability to suppress the biochemical defects seen in mitochondrial metabolism that can result from an mt-tRNAval mutation.
But data presented here could change that.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com