Multitasking β-catenin: from adhesion and transcription to RNA regulation

β-Catenin is an evolutionally conserved protein which orchestrates myriad biological processes by regulating Wnt signaling and cell adhesion. The importance of the dual roles of β-catenin protein (signaling and structural) is highlighted throughout the development and adult life of all metazoan anim...

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Bibliographic Details
Published inAnimal cells and systems Vol. 17; no. 5; pp. 299 - 305
Main Authors Hur, Jung, Jeong, Sunjoo
Format Journal Article
LanguageEnglish
Published Taylor & Francis 01.10.2013
한국통합생물학회
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Summary:β-Catenin is an evolutionally conserved protein which orchestrates myriad biological processes by regulating Wnt signaling and cell adhesion. The importance of the dual roles of β-catenin protein (signaling and structural) is highlighted throughout the development and adult life of all metazoan animals. β-Catenin is located in the cadherin-based adherent junctions in the plasma membrane of epithelial cells; upon Wnt activation, it accumulates and translocates to the nucleus in order to activate transcription. Thus, mutations in β-catenin and the components of the Wnt signal transduction pathway underline the aberrant activation of Wnt/β-catenin signaling in human diseases and cancers. In this review, we briefly summarize the core functions of β-catenin relevant to Wnt signaling and adhesion and introduce the additional and novel role of β-catenin related to the regulation of RiboNucleoAcid (RNA) metabolism. Such multiple functions of β-catenin can be understood by examining its structure and complex with the plethora of interacting proteins. Also, molecular evolution analysis has been used to understand the origin of multifunctionality of β-catenin. We will also discuss the newly identified role of β-catenin as an RNA-binding protein and as a regulator of RNA stability and splicing. It is hoped that future research will shed light on any unexpected findings by clarifying the RNA-mediated mechanism of β-catenin and the implication to Wnt-regulated pathogenesis.
Bibliography:G704-000140.2013.17.5.010
ISSN:1976-8354
2151-2485
DOI:10.1080/19768354.2013.853694