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It seems that the intracellular polyphosphate level is maintained by shifting the equilibrium between the forward and the reverse rate of the enzyme reaction.
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Similarly, upregulation of ppk1 encoding polyphosphate kinase increases polyphosphate levels and enhances activation of the MprAB two-component system [47], mediating a positive feedback loop through SigE [3].
It has been shown that transgenic bacteria expressing ppk has higher polyphosphate levels and higher mercury resistance than untransformed bacteria [ 21, 22].
Other phenotypes resulting from the loss of Kcs1 in yeast cells include defects in DNA repair, vacuole morphology, autophagy, telomere length regulation, cell cycle progression, polyphosphate levels and inositol metabolism [ 5, 6, 18].
On this basis, it is tempting to speculate that the down-regulation of genes responsible for phosphate uptake and phosphate distribution in the cell could be related to the elevated polyphosphate levels in Q56-YFP synthesizing cells.
Polyphosphate addition levels less than 0.4% showed significant effects on product cooking yield, diameter, lipid content, adhesion, viscosity and Hunter-a value, mostly in quadratic forms.
We propose that the activation is due to an increased level of short-chain polyphosphate produced by the cleavage of longer molecules of the polymer.
Examples of TRPM8 modulators are: phosphoinositides [25], PIP2 [26]–[28], phosphorylation [28], [29], inorganic polyphosphate [30] channel density, intracellular Ca2+ levels [27], the variable expression ratio of K+/TRPM8 channels [31], [32] and lipid rafts [33].
In this study, bacterial transformation with transcriptional and translational enhanced vectors designed for the expression of metallothionein and polyphosphate kinase provided high transgene transcript levels independent of the gene being expressed.
The genes flanking SK did not appear to encode related functions, being an ATP-binding cassette protein and a leucine rich protein lying upstream of ska, while genes encoding a homologue of the E. coli relA and spoT genes which moderate levels of guanosine 5',3' polyphosphate during nutritional stress lie downstream [ 71].
These showed that PAOs might prefer to utilize glycogen during the endogenous respiration for maintenance purposes [ 8, 20, 22, 23] and then utilize polyphosphate when the glycogen decreased to a certain level.
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