IndraLab

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"The KCNQ1 ion channel inhibitor chromanol 293B caused membrane depolarization, redistribution of beta-catenin into the cytosol, and a reduced transepithelial electrical resistance, and stimulated CRC cell proliferation."
28373572
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"Therefore, activation of the KCNQ1 potassium channel and increased SOS1 expression promote the fibrogenic response and proliferation and migration of gingival fibroblasts through the Ras/Raf/MEK/ERK pathway."
37752101
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"We deduced that ZNF513 mutation led to the elevated expression of KIF3C and SOS1; meanwhile, KIF3C mutation led to the activation of PI3K and elevated KCNQ1 expression, which led to accelerated fibrosis of gingival fibroblasts and the enhanced proliferation and migration of fibroblasts, and finally led to the development of gingival fibromatosis (Fig. 8)."
37752101
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"KCNQ1 ion channel inhibitor Chromogen 293B causes membrane depolarization, redistribution of β-catenin into the cytoplasm, reduces transepithelial resistance, and stimulates CRC cell proliferation."
35836256
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"The m6A demethylase ALKBH5-mediated m6A modification of lncRNA KCNQ1 overlapping transcript 1 promotes the proliferation, invasion, and metastasis of laryngeal squamous cell carcinoma cells by upregulating HOXA9 [33]."
36982798
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"LncRNA KCNQ1OT1 is an imprinted antisense lncRNA in the human KCNQ1 locus ( Kanduri, 2011 ), which was reported to promote proliferation and epithelial-mesenchymal transition of epithelial cells ( Che[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
30703347
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"For instance, lncRNA KCNQ1 opposite strand/antisense transcript 1 was found to be overexpressed in BC tissues compared with normal bladder tissues and can promote cell proliferation, migration, invasion, and apoptosis via modulating the miR-218–5p/HS3ST3B1 axis (Li et al., 2020a)."
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"In AE there is evidence that K + channels may be involved in alveolar epithelial cell repair processes [XREF_BIBR], since the inhibition of K ATP and KvLQT1 K + channels reduces wound healing, cell migration, and proliferation in a model of mechanical injury of primary cultured rat ATII cells [XREF_BIBR]."
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