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Although it was not assessed experimentally, it is possible that these downregulated genes would be upregulated in response to excess Fe.
Based on in vitro evidence that 1α-OHase expression in macrophages is induced by TLR recognition of bacteria [6], [8], [19], we hypothesized that 1α-OHase expression would be upregulated in both macrophages and mammary tissue during a mammary infection.
Based on our findings that TMEM135 is highly expressed in VLCAD mice at birth (when lipid stores are strongly mobilized), and given a potential role for TMEM135 in fatty acid oxidation, we hypothesized that TMEM135 protein levels would be upregulated upon physiological stresses such as cold exposure and fasting (conditions in which fat stores and fat utilization are required).
Thus, genes involved in non-fermentative modes of metabolism would be upregulated at the same time as glucose levels drop.
We hypothesised that RRM2 and TOP2A expression would be downregulated in drug-resistant cells, whereas TOP2B expression would be upregulated.
If the cells produced more ceramides (forming the backbone of sphingolipids) at low oxygen levels, at least one of these two genes would be upregulated.
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Despite lignin formation resulting from a complex network of interacting genes, we anticipated that CAD would not be upregulated.
We thus tested the hypothesis that UCP2 expression would not be upregulated if ROS were scavenged at the appropriate time, i.e. beginning at the time of the preconditioning ischemia.
The inflammation observed microscopically in birds affected with Wooden Breast suggests that genes involved in the coagulation system pathway would likely be upregulated due to vascular (venous) damage and inflammation.
Glycolysis and lactate fermentation would need to be upregulated in these tumor cells in order to compensate for the absence of OxPhos.
Accordingly, Gsc expression would be expected to be upregulated upon Vent1/2 depletion.
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