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The ability of the C-terminal mtLeuRS to suppress functional defects caused by tRNA mutations is intriguing, but the mechanism of rescue is still controversial.
The pluripotent condition may thus be viewed as a transcription factor battlefield in which Oct4, Sox2, and Nanog are dominant and continuously suppress functional expression and activity of lineage specification factors (Niwa, 2007; Smith, 2005) Crucially, however, Oct4 and Sox2 also provide for developmental extinction of pluripotency by directing expression of FGF4.
How RNAPII from an interfering promoter is able to suppress functional transcription of the overlapped promoter remains to be determined, but stalling of the interfering RNAPII elongating over the sensitive promoter has been suggested to block access of essential TFs [ 30, 83].
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Although there were significant differences in the improvement of motor functions between muscimol-treated and vehicle-treated mice, the time points, when the significantly suppressed functional recovery was observed in the muscimol-treated mice, were different in these two tests.
Bromoethanesulfonate, animal-vegetable fat, and monensin were compared with a control treatment to suppress different functional groups of ruminal prokaryotes in the presence or absence of protozoa to evaluate changes in fermentation, digestibility, and microbial N outflow.
Our finding is also in contrast to the recent study showing endogenous trkB ligands (BDNF and NT4) suppress the functional mechanosensory plasticity (sprouting) in the deafferented spinal cord [58].
It is therefore possible that stimulating expression of SUR2A over the levels of Kir6.2 expression would suppress the functional expression of KATP channels from optimized dimeric SUR2A/Kir6.2.
Dominant-negative mutations will suppress the functional activity of any wild-type p53 that is present, leading to loss of normal protective mechanisms.
Previous studies have reported that intratumoral Treg cells can suppress the functional capabilities, proliferation, production, and secretion of IFN-γ and interleukin (IL -4 of autologous IL -4trating CD4+CD25− T cells [ 21].
In in vitro studies, PER1 overexpression suppressed chondrocyte differentiation by suppressing a functional E-box in the Ihh promoter.
Transcription from the p16INK4a promoter is suppressed by functional pRb (Li et al, 1994), whereas expression of functional p16INK4a induces downregulation of pRb transcription (Fang et al, 1998).
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