IndraLab
Statements
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"Curcumin inhibited BCSCs migration by inhibiting beta-catenin nuclear translocation, attenuating the expression of beta-catenin transcriptional targets including pro EMT factors, along with the increased formation of E, cadherin, beta, and catenin complex and suppressed expression of epithelial markers."
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"Wang et al. reported that an increase in mRNA expression of beta-catenin and axin2 in kidney tissues of patients with lupus nephritis compared with control kidney tissues, accompanied by an increase of beta-catenin protein expression XREF_BIBR Their study also showed that beta-catenin mRNA expression was significantly higher in lupus nephritis patients without renal interstitial fibrosis compared to those with renal interstitial fibrosis and increased beta-catenin mRNA expression positively correlated with the creatinine clearance rate (Ccr)."
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"HONE1 hybrid cells with infected beta-catenin shRNA have reduced expression of beta-catenin and representative results from various passages of cell populations after infection of shRNA plasmids are shown in the bottom panel, Figure XREF_FIG A. beta-catenin expression was reduced by approximately 54%, 97%, 70%, and 79% in MCH4.5 and MCH4.6 cell lines at different passage levels after infection."
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"Activation of beta-catenin transcription by APC mutations or mutations of beta-catenin itself is not functionally equivalent to an up-regulated Wnt initiated signalling because Wnt activates, except for the canonical beta-catenin pathway another pathway that through kinases Tak1 and Nlk (Nemo like kinase) phosphorylates and inhibits TCF4 [XREF_BIBR] finely tuning transcriptional activity under physiologic conditions."
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"MP has been shown to up-regulate the expression and activation of the beta-catenin signaling pathway, including low-density lipoprotein receptor related protein-6 (LRP) pho sphorylation, beta-catenin, and glycogen synthase kinase-3beta (GSK) phosphorylation (XREF_FIG) [XREF_BIBR]."
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"Alternatively, the interaction between E-cadherin and beta-catenin at the adherens junction raises the intriguing possibility that the loss of E-cadherin function may actively regulate the levels of free beta-catenin, thereby altering its ability to regulate target genes that support tumor invasion."
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"Our results showed that the transfection of CTNNB1 T41A or S45F mutation had no effect on the expression of total beta-catenin; however, the transfection of CTNNB1 S45F mutation induced the nuclear expression of beta-catenin, suggesting that this specific mutation might affect beta-catenin translocation to the nucleus independent of cell type."
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"The results are in concordance with previous studies where beta-catenin protein levels have been found to be downregulated XREF_BIBR and the beta-catenin and hTcf -4 nuclear complex reduced XREF_BIBR upon Zn stimulation in HT29-APC cells indicating, decreased levels of nuclear beta-catenin."