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The differential expression profile between naive wild-type and mutant cells involved several thousand genes.
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These results imply that programmed cell death triggered by JAK2 inhibition in the JAK2V617F mutant cell lines involves both the intrinsic and extrinsic pathways.
When cells with a normal copy of the KRAS gene were exposed to the contents of the exosomes released from KRAS mutant cells, an important gene involved in cell growth was suppressed.
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].
It involved transfecting mutant cells with candidate genes, exposing them to IFN, preparing RNA and then using RNase protection assays to test whether the induction of IFN-dependent gene expression had been re-established.
Development of mammary tumours involves accumulation of mutant cells caused by excessive proliferation and insufficient apoptosis or dysregulation of cellular differentiation.
How the scrib mutant cells are recognised is currently unknown, but might involve changes in cell morphology.
Repair of these DSBs likely occurs in a process involving Ku and Ligase IV, since mutant cells show an extreme sensitivity to etoposide [36], [37], [38].
Mutant cells deficient in both talin A and talin B, actin-binding proteins involved in cell-substratum adhesion, also cannot attach to the substratum (Tsujioka et al., 2008).
Nearly every step of ommatidial assembly involves Notch signaling [49], [50], and so elimination of the Notch pathway in clones of mutant cells is catastrophic to eye development.
The results suggested that an induction mechanism was involved in the regulation of β-Xylosidase biosynthesis which enhanced specific yield of enzyme (Yp/x) up to 59-fold in the mutant cells (Rajoka and Khan 2005).
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