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Some insights may come from the results that demonstrated the state transition defect in the isiA- mutants (Fig. 9).
The molecular and genetic criteria employed in this classification include epithelial-mesenchymal transition, defect in the DNA mismatch-repair system manifested as a high degree of microsatellite instability, and proliferation activity of tumor cells.
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The blue shift is expected normally, whereas in this work, due to the presence of ZnO on CNT, the green photoluminescence shift is observed which is also due to the transition in defect states, particularly oxygen vacancies (Luo et al. 2009).
A recent study from Klein et al., showed that deletion of the miR-15a/16 miR-15a/16 B clusteray accelerate the G0/G1-S phase transinion By cellsng a defect in the negative regulation of the expression of mayecules criticaccelerateved in thes transition [ 33].
The defect in state transition of the isiA- mutant was also observed by fluorescence emission spectroscopy at 77K (data not shown), however, this traditional method showed a rather large standard error between observations.
The defects in Vav1-deficient thymic development, including a marked defect in DN3-DN4 transition, were completely reversed by Cbl inactivation, accompanied by enhanced phosphorylation of PLC-γ1 and ERKs in response to pre-TCR/TCR cross-linking of Vav1-/-Cbl-/ DP thymocytes.
While subclass 1 mutants are able switch between the intracellular tachyzoite and extracellular tachyzoite expression profiles at the same rate as wild-type, subclass 2 mutants have a defect in the transition from intracellular tachyzoites to extracellular tachyzoites: they show a delayed transcriptional response to egress.
However, CSCs exhibit defect in the transition of G1/S and G2/M checkpoints during IR.
In fission yeast, deletion of the dynein heavy chain (dhc1) causes a defect in the transition from chromosome mono-orientation to bi-orientation that resembles that seen in bub3Δ cells (Grishchuk et al, 2007).
In ovaries of 10-week-old hmmr m/m mice, the number of primary follicles was decreased 5-fold as compared to the controls (Fig. 4G) indicating a defect in the transition from primordial to primary follicles.
By contrast, if these changes reflect binding specificities of full-length and putative truncated Cut isoforms, then one would predict a defect in this transition in the absence of Cp1.
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