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Learn MoreWe previously identified miR-1343 as a potent repressor of TGF-b signaling and fibrosis through the direct attenuation of both canonical TGF-b receptors. Here, we build upon our previous findings to better characterize the function of endogenous miR-1343 in normal biology. CRISPR/Cas9 techniques were used to delete the miR-1343 locus in A549 lung epithelial cells. Loss of miR-1343 was found to impact several processes and genes implicated in fibrosis and known to be TGF-b pathway effectors. These responses are opposite to those we observed previously when miR-1343 was overexpressed in the same cell type. SOURCE: Ann HarrisAnn Harris Lab Case Western Reserve University
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