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The rapid and coordinated repression of histones and M/G1-specific transcripts cannot be explained by cell cycle arrest, and suggested that there are additional signaling pathways that directly repress these genes in cells under genotoxic stress.
The different phenomenon could be explained by cell penetration rate of the nanoscaled drug delivery systems depending on the NP concentration differences between the internal and external environment of the cell membrane or the interaction of the NPs and the cell membrane.
The DO reduction could be explained by cell growth, reproduction, and thus elevated respiration.
These differences could be explained by cell type or fusion protein system specificity mediating localization due to differences in cell signaling and protein interaction.
Alternatively, neurons derived from bone marrow stromal cells after transplantation could be explained by cell fusion, giving rise to uncertainties over "real" transdifferentiation [36], [37].
These contradictory results may be explained by cell competition, mentioned above (Levayer and Moreno 2013).
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This can be explained by cells on the "favourable" 15 nm regions that strongly produce and shed extracellular matrix onto the "unfavourable" locations.
This could be explained by cell-type heterogeneity of its imprinted status in the placenta.
These binding differences can partly be explained by cell-type specific regulation.
BET proteins, in particular BRD4, play essential roles in cell-cycle progression (You et al., 2009) and mitosis (Zhao et al., 2011), thus raising the possibility that BET inhibitor effects on ESC pluripotency could be explained by cell-cycle arrest and compromised cell viability.
While this preference for particular tumor types can be explained by cell-specific factors affecting L1 mobilization, there is also significant variation in the extent of L1 mobilization within cancers of the same type that could be due to differences in polymorphic, active L1 elements between two individuals [ 27, 40].
More suggestions(18)
be characterized by cell
be explained by tissue
be described by cell
be explained by cells
be modelled by cell
be explained by demand
be employed by cell
be explained by tolerance
be regained by cell
be explained by reselling
be quantified by cell
be reached by cell
be done by cell
be evaluated by cell
be normalized by cell
be restricted by cell
be normalised by cell
be explained by path-dependence
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