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In many tissues, Notch signalling contributes to the maintenance of stem cells or precursor cells [ 10] and pathway hyperactivation caused by point mutations [ 11] or translocations involving NOTCH genes [ 12, 13] is oncogenic by blocking cell differentiation, protecting against apoptosis and stimulating proliferation.
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These toxins, termed cyclomodulins, can promote cell proliferation or, conversely, inhibit cell growth and modulate differentiation by blocking cell cycle progression [1], [2].
By blocking cell division from the gastrula stage, we show that cell proliferation is not essential for differentiation of cardiomyocytes, and the resulting heart remains essentially normal in size, as determined by the expression of markers of cardiac differentiation.
First, it downregulates the basal cell phenotype and promotes differentiation by upregulating expression of differentiation markers and blocking cell cycle progression (Rangarajan et al., 2001; Moriyama et al., 2008; Restivo et al., 2011).
In addition to abrogating the function of regulatory cells by blocking their differentiation, accumulation of regulatory cells in the tumour microenvironment can be reduced by targeting chemokine pathways.
In summary, elevated Pja2 expression can inhibit TGF-β signaling and therefore is likely to maintain neural crest cells in their progenitor state by blocking their differentiation into noradrenergic cells.
JARID1B displays an important yet complex role in stem cell biology by blocking differentiation in embryonic and hematopoietic stem cells [ 172, 173], however in a different study it was found to be dispensable for embryonic stem cell maintenance and critical for neural differentiation [ 174].
This model for BMP function is supported by studies on the drosophila ovariole in which BMP signals produced from niche cells maintain self-renewing germline stem cells by blocking differentiation (Kai & Spradling, 2004; Song et al, 2004).
Dey, B. K. et al. The histone demethylase KDM5b/JARID1b plays a role in cell fate decisions by blocking terminal differentiation.
γ-Irradiation after an initial proliferation phase induced by CD40 ligand and immediately prior to initiation of the differentiation phase blocked cell growth but did not affect cell viability or plasma cell differentiation.
There is increasing evidence that PRC complexes have a role in tumor progression and development by blocking differentiation and promoting stem cell self-renewal.
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