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It has been previously shown that MYCN may mediate proliferation in NB through association with the promoter regions of the minichromosome maintanence complex genes (MCM), resulting in increased expression [8].
This suggests that oestrogen may mediate proliferation of hPASMCs and may contribute to PAH pathology.
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Furthermore, TP53INP1 might be a target gene of miR-155 in fibroblasts, which may mediate the proliferation and the activation of normal fibroblasts, and manifest the characteristics of CAF.
While these data don't exclude the possibility of a paracrine regulation of cell proliferation by ERα in these cells, the colocalization of ERα and Ki-67 does support the hypothesis that ERα may mediate cell proliferation in an autocrine mode in these ERα-positive breast cancer cell lines, a mechanism absent in normal mammary cells and most primary breast tumors [ 1- 3, 16- 18, 23, 24].
The presence of chronic inflammation suggests that the immune system may mediate mammary lesion proliferation through systemic or local regulation of cytokines and/or growth factors.
Using gene expression profiling we were able to identify a candidate that may mediate the PC2-induced proliferation in PKD2(1 703) rat.
In addition, the finding that IGF-1 and IGF-2 expression is correlated with the expression of both estrogen receptors is consistent with the idea that IGF expression is regulated by estrogen, and IGF may mediate estrogen-induced cell proliferation in the endometrium [ 13].
Rather, c-FLIPL may mediate T cell activation and proliferation via an unidentified mechanism 7. c-FLIPL may therefore serve as a modulator between apoptotic and proliferative responses after T cell receptor (TCR) stimulation 9.
Osteopontin is an extracellular matrix protein that contributes to the development of atherosclerosis as it acts as a pro-inflammatory cytokine to induce macrophage adhesion and migration, it promotes vascular smooth muscle cell proliferation and may mediate vascular calcification [ 29].
Regarding the adult liver-enriched miRNAs, similar to let-7, miR-23b is capable of inhibiting cell proliferation [44], and may mediate cell cycle arrest in mature hepatocytes.
Therefore, oscillatory activity of carnitine O-acetyltransferase may mediate prechondrogenic condensation by modulating cellular proliferation.
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