Short CommunicationLocalization of the Human β-Catenin Gene (CTNNB1) to 3p21: A Region Implicated in Tumor Development
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Arsenic-induced mutagenesis and carcinogenesis: A possible mechanism
2023, Handbook of Arsenic ToxicologyExploring the structural significance of molecular switch mechanism alias motif phosphorylation in Wnt/β-catenin and their crucial role in triple-negative breast cancer
2021, Archives of Biochemistry and BiophysicsCitation Excerpt :Recent studies show the increased evidence Wnt/β-Catenin signaling activation associated with high TNBC progression among other mechanisms [1–3]. β-Catenin is a multifunctional protein located to the intracellular side of the cytoplasmic membrane coded by the CTNNB1 gene, which maps to chromosome 3p22.1 [4]. The general structure of β-Catenin comprises of three domains, (i) the N - terminal (residues:1–137) domain initiate signaling cascade, (ii) a central domain (residues: 138–664) combined with 12 armadillo repeat domain (R1-R12) also known as ARM assembled with helices and superhelices via fold back mechanism for cell adhesion (iii) the C - terminal (residues: 665–781) domains are believed to regulating proteasomal degradation [5–7].
Probing the chemoprevention potential of the antidepressant fluoxetine combined with epigallocatechin gallate or kaempferol in rats with induced early stage colon carcinogenesis
2021, Journal of Pharmacological SciencesCitation Excerpt :This procedure was based on the reduction of nitrate by vanadium III chloride (VCl3) to nitrite that combined with detection of NO by Griess reaction.37 β-catenin is a multifunctional protein complex that is involved in regulation and coordination of cell–cell adhesion and gene transcription.38 The serum and tissue β-catenin were estimated by utilizing the commercially available Invitrogen™ β-catenin (Invitrogen, Camarillo, CA, USA) rat ELISA kits.
Aberrant β-catenin expression in urothelial carcinomas in blackfoot disease-endemic areas
2017, Kaohsiung Journal of Medical SciencesCitation Excerpt :During tumorigenesis, when E-cadherin expression on cell surfaces is decreased or when proteasomal degradation of cytosolic β-catenin is inhibited, β-catenin in cytoplasm accumulates and then migrates into the nucleus. Interaction between β-catenin in the nucleus and downstream transcription factors causes abnormal activations of downstream genes [16]. Mutations and overexpression of β-catenin are associated with a poor prognosis in many cancers, such as bladder cancer, hepatocellular carcinoma, and colorectal cancer.