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Inactivation of Rfx1 occurs in response to DNA damage and causes the induction of many genes [ 31] (by release of repression by Rfx1).
This phenomenon can be explained by the fact that translationally repressed gap50 transcript is present in the non-activated gametocytes (see above), and that the release of repression during activation leads to rapid translation and in consequence to a loss in transcript abundance and an increase in protein abundance.
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PER1 and PER2 are phosphorylated at multiple sites by CK1δ and CK1ε that facilitates their degradation and subsequent release of inhibitory repression of Clock/BMAL1 as key elements of the cell-autonomous transcription translation feedback loops [91, 92].
Further, simultaneous inhibition of both these pathways lead to release of the repression by almost about 60% (Fig. 4D).
These data demonstrate that Gal4 and Gal4-VP16 acanvity can be repressed in a dose-dependant manner with morpholinos, and that the eventual release of this repression following morpholino degradation allows postembryonic expression of Gal4-driven transgenes.
An essential part of hedgehog pathway activation involves release of Ptc1 repression of Smo.
Release of MYB repression promotes an epithelial phenotype, or MET, in which proliferation is restored.
Consequently, PYK-mediated regulation of respiration was additive to the release of glucose repression and is thus an independent process.
Moreover, the release of glucose repression and increased inulinase activity at the initial stage of fermentation, by controlling the transcription factor Mig1, may help to improve productivity.
Furthermore, reduced PYK activity and a release of glucose repression provoked a similar mRNA expression fingerprint on studied enzymes of oxidative metabolism.
Induction of Sko1-dependent genes requires the release of this repression, and this process is completely dependent on Hog1 (Pascual-Ahuir et al. 2001; Proft and Struhl 2002).
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