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The incorporation of H2B-GFP into chromatin may affect gene expression profile and cell fate commitments via multiple mechanisms including effects on nucleosome structure, chromatin structure, histone code, epigenetic regulation of gene expression, asymmetric cell division and potential "leakiness" of the doxycycline-inducible system itself.
Particularly, the activation of the small GTPase RhoA and its direct effector protein, ROCK, have vital roles in MSC fate commitments between the adipogenic, chondrogenic and osteogenic lineage pathways [23], [64] [66] and have been demonstrated to have a necessary role in mechanically induced osteogenic differentiation [23].
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The mechanism described here may be more general than expected and could account for how murine cells after fate commitment like the secretory-committed cells defer for long periods their terminal differentiation (Buczacki et al, 2013).
The derived Schwann cells used were checked for fate commitment.
Our results provide new insights into epigenetic mechanisms underlying properties of pluripotency and cell fate commitment.
Here, we find that architectural constraints on noise suppression are overcome to stabilize fate commitment.
It is well known that topographical and biochemical signals play crucial roles in modulating cell fate commitment.
Understanding the logic of nuclear architecture and how it contributes to differentiation and cell fate commitment remains challenging.
These results together provide information of the stem cell fate commitment on hierarchical structure and a promising approach to design advanced biomaterials by focusing on specific mechanotransduction process.
In our study we used myoblasts that express the differentiation marker CD56 considered as a sign of definitive fate commitment to the muscle pathway.
After fate commitment to ILC2 lineage, Bcl11b is also required for the maintenance of ILC2 identity, mainly through positive regulation of Gfi1 and Rora expression, and negative regulation of Ahr expression.
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