IndraLab

Statements

Mutated CTNNB1 increases the amount of CTNNB1. 9 / 9
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"Our data suggest that CTNNB1 mutations that increase beta-catenin protein levels sensitize cells to navitoclax."
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"Altogether, the results showed that beta catenin mutations found in HCCs generated by TCPOBOP alone, unlike those observed in HCCs from DENA-TCPOBOP-treated mice, do not induce the transcription of cl[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Given that CTNNB1 mutations lead to aberrant β-catenin expression—a major downstream effector of the Wnt pathway associated with poorer overall survival (OS) in various cancers43—this finding underscores the relevance of the β-catenin pathway in EMC-associated tumorigenesis."
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"However, APC inactive or hyperactive β-catenin mutants may drive aberrant activation of β-catenin and excessive transcription of Wnt downstream targets, including c-Myc, Cyclin D1, EpCAM, Snail, and Twist, which consequently cause physiological and pathological disorders, including cancer [20,21]."
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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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"Mutation of beta-catenin, APC or Axin found in several human cancers was reported to cause elevated beta-catenin levels and yield inappropriate activation of TCF target genes such as c-Myc and cyclin [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Gain-of-function CTNNB1 mutations lead to nuclear overexpression of β-catenin, which is a core component of the canonical Wnt/β-catenin pathway [3]."
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"The results showed that CTNNB1 mutations induced a higher expression of CTNNB1, and target genes included GLUL, c-myc and TCF-1 ( Fig. 5 A )."
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"To this end, we generated HG HRECs that stably expressed a doxycycline-regulated, constitutively active β-catenin mutant cDNA.15 Addition of doxycycline first increased the level of β-catenin mRNA, and then elevated the level of β-catenin protein (Figs."
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