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In addition, the amplitudes of the fast and slow peak in the kinetics of the delayed light emission and non-photochemical fluorescence quenching ( NPQ) were significantly reduced in mutant cells, indicating low level of the membrane energization of photosynthetic membranes.
Conversely, significant levels of G-CSF were found in the supernatants of mutant cells, indicating that STAT5−/− LSECs are capable of releasing high amounts of G-CSF without external stimulation.
However, the level of TUNEL staining was not uniformly elevated in the mutant cells, indicating that there is no increase of DNA damage compared to wild type.
Interestingly, a significant reduction in polysaccharide secretion was observed in the mutant cells, indicating inositol utilization plays a role in cell surface capsule production.
However, the nuclear envelope diffusion barrier is not affected in the bud1Δ mutant cells, indicating that assembly of the nuclear barrier is controlled differently.
Interestingly, a significant reduction in glucuronoxylomannan (GXM) secretion was observed in the itr1aΔ itr3cΔ mutant cells, indicating that inositol utilization pathways play a role in capsule production.
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Ultrastructural analysis of slpA mutant cells indicated loss of much of the outer Hpi protein carbohydrate coat, the 'pink envelope', and the membrane-like backing layer.
Decreases in lysophospholipids 18 0 (lysoPI 18 0, lysoPE 18 0, lysoPC 18 0, and LysoPG 18 0) in CST26 mutant cells indicated alternative pathways to sequester lysophospholipids, which would be expected to increase in cells lacking Cst26p.
Evaluation of chronologically aged bat1Δ bat2Δ mutant cells indicated that the intracellular accumulation of trehalose is not significantly different from that of the wild-type strain.
However, the Telomerase- phenotype of the tel1 mec1 double mutant cells indicates that the Mec1p kinase also plays a role in telomere function.
Expression profiling of pog1Δ and other mtDNA-less mutant cells indicates that genes involved in glycolytic pathways and stress response are induced, common to budding yeast and human cell line systems [ 22- 24].
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