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We report here for the first time that temperature downshift is beneficial for effective control of the acidic peak variant content.
Combination of induction temperature downshift with the glycyl-tRNA pool increase in E. coli led to enhanced biosynthesis of glycine-rich silk proteins.
However, Mia1p-GFP accumulated in the nuclei of interphase crm1-809 cells at the restrictive temperature of 18°C (nuclear Mia1p-GFP signal increases ∼90%, n = 50 cells, p<0.01 upon temperature downshift).
Temperature downshift restores normal BMP signaling, allowing normal lineage differentiation after clonal induction.
One study reported that opuCA transcript levels are unaffected during temperature downshift or growth at 4°C [ 17], while another study observed that opuCA transcription is induced after temperature downshift [ 13].
Recombinant expression was induced by a temperature downshift to 15 °C and addition of 0.4 mM IPTG.
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These findings strongly suggest that lipid metabolism and fatty acid changes in strain N33 might be essential for the adaptation to temperature downshifts.
Microorganisms differ in responding to a sudden downshift in temperature and this, in turn, impacts their metabolic processes and can cause various structural modifications.
This promoter drives high levels of protein expression, comparable to the commonly used T7-system, but is induced by a downshift in temperature rather than addition of an exogenous chemical inducer [ 9, 10].
In contrast, the high expression of cheA-1 (red triangles) tended to occur earlier in response to environmental stress: over a period of 5-20 min after the downshift of temperature, and over a period of 20 min after IR exposure.
Recently, activation of the HOG pathway upon a downshift in temperature (30 to 12°C) was monitored in S. cerevisiae, whereas in Schizosaccharomyces pombe the Sty1p MAP-kinase (the Hog1p homolog) lead to the activation of several cold-induced genes [ 35, 36].
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