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Its expression in C2C12 cells recapitulates key features of the FSHD molecular phenotype, including repression of MyoD and its target genes, diminished myogenic differentiation, repression of glutathione redox pathway components, and sensitivity to oxidative stress [23].
During ES cell differentiation, repression of Oct4 and Nanog is essential, considering that ectopic expression of Oct4 can block differentiation, while expression of Nanog is enough to maintain ES cell self-renewal and pluripotency, even in the absence of extrinsic factor LIF or Oct4 expression [44], [45], [62].
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Cell cycle exit also plays an important role in differentiation, and repression of one of the downregulated CDKs, CDK6, has been linked to leukemic differentiation [43, 44].
Thereby, we propose that PKD2 functions in a dual mode of myoblast differentiation (i) repression of self-renewal and (ii) induction of differentiation.
Recent study indicate that NO pathways that promote CM differentiation include repression of self-renewal genes, such as NANOG, and increase in differentiation genes such as GATA4 [27].
In the mammalian skin as well as during T helper cell differentiation, target repression by RBP-J does not play an important role [46], [47], suggesting that in these tissues Notch signals in an RBP-J independent manner.
BCL6 was shown to promote follicular helper T-cell differentiation through repression of multiple miRNAs.
Results suggest that miR-146 regulates NSC differentiation through repression of Notch 1 expression.
The role of PcG in cell differentiation through repression of target genes is well acknowledged.
During the process of neural differentiation, the repression of neuroectodermal genes is attenuated, which is accompanied by an increase in acetylation of target genes.
Thus, we reveal a novel mechanism by which GATA-1 secures TPO signaling-induced ERK activation to ensure megakaryocyte differentiation through repression of the negative regulator PSTPIP2 in normal megakaryopoiesis.
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