منابع مشابه
Axin localizes to the centrosome and is involved in microtubule nucleation.
Axin is known to have an important role in the degradation of beta-catenin in the Wnt pathway. Here, we reveal a new function of Axin at the centrosome. Axin was localized to the centrosome in various cell lines and formed a complex with gamma-tubulin. Knockdown of Axin reduced the localization of gamma-tubulin and gamma-tubulin complex protein 2-components of the gamma-tubulin ring complex-to ...
متن کاملA Drosophila Axin homolog
Like in many other signaling pathways, most components in Wnt signal transduction are highly conserved in evolution. In organisms ranging from C. elegans to mice, a similar hierarchy of signaling molecules transmits the Wnt signal to the nucleus. In current models of this pathway, the secreted Wnt protein is received by Frizzled-like cell surface receptors. In the cytoplasm, Dishevelled (Dsh) r...
متن کاملRapid, Wnt-Induced Changes in GSK3β Associations that Regulate β-Catenin Stabilization Are Mediated by Gα Proteins
Background: In the absence of Wnt stimulation, the transcriptional cofactor b-catenin is destabilized via phosphorylation by protein kinase GSK3b in complex with Axin family members. In the ‘‘canonical’’ Wnt signaling pathway, Disheveled (Dvl) is required to functionally inhibit the activity of the GSK3b/Axin complex and thereby stabilize b-catenin. Yet, the mechanisms that underlie Wnt regulat...
متن کاملInteraction of axin and Dvl-2 proteins regulates Dvl-2-stimulated TCF-dependent transcription.
Axin promotes the phosphorylation of beta-catenin by GSK-3beta, leading to beta-catenin degradation. Wnt signals interfere with beta-catenin turnover, resulting in enhanced transcription of target genes through the increased formation of beta-catenin complexes containing TCF transcription factors. Little is known about how GSK-3beta-mediated beta-catenin turnover is regulated in response to Wnt...
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ژورنال
عنوان ژورنال: Atlas of Genetics and Cytogenetics in Oncology and Haematology
سال: 2011
ISSN: 1768-3262
DOI: 10.4267/2042/38411