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HuR regulates gap junctional intercellular communication by controlling β-catenin levels and adherens junction integrity by Niloofar Ale-Agha; Stefanie Galban; Christiane Sobieroy; Kotb Abdelmohsen; Myriam Gorospe; Helmut Sies; Lars-Oliver Klotz is a Medicine article available to read on EtoBox.
What is HuR regulates gap junctional intercellular communication by controlling β-catenin levels and adherens junction integrity about?
Gap junctional intercellular communication (GJIC) plays a critical role in the regulation of tissue homeostasis and carcinogenesis and is modulated by the levels, subcellular localization, and posttranslational modification of gap junction proteins, the connexins (Cx). Here, using oval cell-like rat liver epithelial cells, we demonstrate that the RNA-binding protein HuR promotes GJIC through two mechanisms. First, HuR silencing lowered the levels of Cx43 protein and Cx43 messenger RNA (mRNA), and decreased Cx43 mRNA half-life. This regulation was likely due to the direct stabilization of Cx43 mRNA by HuR, because HuR associated directly with Cx43 mRNA, a transcript that bears signature adenylate-uridylate-rich (AU-rich) and uridylate-rich (U-rich) sequences in its 3'-untranslated region. Second, HuR silencing reduced both half-life and the levels of beta-catenin mRNA, also a target of HuR; accordingly, HuR silencing lowered the levels of whole-cell and membrane-associated beta-catenin. Coimmunoprecipitation experiments showed a direct interaction between beta-catenin and Cx43. Small interfering RNA (siRNA)-mediated depletion of beta-catenin recapitulated the effects of decreasing H
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- Author
- Niloofar Ale-Agha; Stefanie Galban; Christiane Sobieroy; Kotb Abdelmohsen; Myriam Gorospe; Helmut Sies; Lars-Oliver Klotz
- Publisher
- Ovid Technologies (Wolters Kluwer Health)
- Published
- 2009
- Language
- EN
- Field
- Medicine (Health Sciences)