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Exposure of plant cells to such fragments induces them to produce antibiotics known as phytoalexins.
The vulnerability of the eIF2B-mutated glial cells to such threat is evident by their propensity to apoptosis (Fig. 3B) albeit a heightened stress response.
As shown in Fig. 2A, LNA oligoes efficiently depleted miR-221 and mir-222 from PC3 cells, to such an extent that miR-221/222 expression was almost undetectable by Northern blot.
The commitment of mouse and human CD4+ T cells to such distinct phenotypes is directed through expression of lineage specific transcription factors, e.g., Tbet for Th1, GATA3 for Th2, and RORγt for Th17 cells [5] [7].
We postulated that there were likely to be differences in the initial molecular responses of cells to such exposures that may drive the differences in cellular response.
To understand why some cancer patients respond better to ionization therapy and drug treatment, several groups have investigated the underlying cellular response of tumor cells to such treatments.
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The effect of large numbers of branches is to expand the cell to such an extent that a mobile rotator phase is induced i.e. the system forms a dynamic rotationally disordered crystal in which chain sliding occurs readily.
Rather, the observed differences in proteasomal transcription profiles would seem to reflect a tolerability of the cell to such variation.
The failure of cells to repair such damage, in individuals with certain biochemical disorders, leads to serious skin problems.
The key cells to generate such cross-presentation are DCs.
Exosomes are microvesicles secreted from cells to biofluids such as blood, urine, and cell culture medium.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com