
IndraLab
Statements
reach
"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]."
reach
"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."