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The in vitro culturing of neuroepithelial stem cells has become an indispensable tool for studying the mechanisms controlling proliferation, mitotic arrest, and lineage commitment of cells in the nervous system.
The question remains as to what causes the delay to the commitment of cells to the first round of proliferation.
The proliferative stage of the disc is accompanied by the specification of different territories, and by the commitment of cells to specific cell fates [2].
Nkx-2.5 is the earliest known marker of the cardiac lineage, and is expressed together with the cardiogenic commitment of cells from anterior-lateral mesoderm [17], [18].
Therefore, our results show that PKCδ-nuclear translocation is an essential key step to prime the sequence of molecular events which culminate in the late caspase 3 activation and in the irreversible commitment of cells to apoptosis.
We have thus revealed early luminal commitment of cells that are morphologically indistinguishable from stem cells.
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Therefore, we propose that Fam20a is primarily expressed in cells committed to the granulocytic lineage and presumably plays a role in either lineage commitment of cell proliferation.
Therefore, the results indicate that commitment of cell fate is determined upon initial expression of p53 or SirT3.
Therefore, it has been proposed that the stress-induced phosphorylation of p53 at Ser-46 is one of the critical events for commitment of cell fate into apoptotic cell death [40], [41].
In this way, all changes of genes and important networks for commitment of cell fate, implementation of differentiation programs, specification and survival were revealed.
Apoptosis is a cell suicide programme characterised by unique cellular events such as mitochondrial fragmentation and dysfunction, nuclear condensation, cytoplasmic shrinkage and activation of apoptotic protease caspases, and these serve as the noticeable apoptotic markers for the commitment of cell demise.
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