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Moreover, 5271 transcripts were regulated (830 up regulated, 4313 down regulated, 128 with inverse regulation) by both high temperature and drought stress.
These results suggest that β-catenin causes mitochondrial dysfunction in NEFH down-regulated cells by inverse regulation of PDH and PK-M2.
Interestingly, for the protein fate group, 3 genes out of the 11 found were up-regulated in the early stage, while 9 genes out of 13 were up-regulated in the middle stage, suggesting a coordinate inverse regulation of protein biosynthesis and fate during these two stages.
We observed an inverse regulation of host and pathogen sucrose transporters by changes in the apoplastic pH.
The different pH-dependences of UmSRT1 and plant sucrose transporters might represent a mechanism for inverse regulation of plant and fungal transporters at the host/pathogen interface.
Our work provides a possible mechanism of how neurogenesis might be influenced, namely by the previously undiscovered inverse regulation of NEUROG2 and KIAA0125 caused by Aβ.
The cluster analysis revealed a previously unknown inverse regulation of NEUROG2 and KIAA0125 in consequence of an inverse Aβ42/Aβ40 ratio.
In these cases our study showed an inverse regulation compared to the proteomics results for functionally linked proteins or for members of a polycistronic operon.
We found that β-catenin was required for the inverse regulation of PK-M2 and PDH by cooperating with deregulated NEFH.
Only two small subsets of genes (8.3% of all, clusters III and IV) displayed inverse regulation between psoriasis and PPARβ/δ mice.
This inverse regulation argues for a specific effect mediated by the Aβ42/Aβ40 ratio itself, because an inverse Aβ42/Aβ40 ratio led to an inverse regulation of this gene and may not be mediated by unspecific effects occasionally observed in microarray studies.
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CEO of Professional Science Editing for Scientists @ prosciediting.com