التفاصيل البيبلوغرافية
| العنوان: |
Nuclear GSK-3β inhibits the canonical Wnt signalling pathway in a β-catenin phosphorylation-independent manner. |
| المؤلفون: |
Caspi, M., Zilberberg, A., Eldar-Finkelman, H., Rosin-Arbesfeld, R. |
| المصدر: |
Oncogene; 6/5/2008, Vol. 27 Issue 25, p3546-3555, 10p, 1 Color Photograph, 2 Black and White Photographs, 4 Graphs |
| مصطلحات موضوعية: |
GENES, WNT genes, TRANSCRIPTION factors, CELL nuclei, CELL lines, GENETIC regulation |
| مستخلص: |
β-Catenin is the central signalling molecule of the canonical Wnt pathway, where it activates target genes in a complex with lymphoid enhancer factor/T-cell factor transcription factors in the nucleus. The regulation of β-catenin activity is thought to occur via a cytoplasmatic multiprotein complex that includes the serine/threonine kinase glycogen synthase kinase-3β (GSK-3β) that phosphorylates β-catenin, marking it for degradation by the proteasome. Here, we provide evidence showing that GSK-3β has a nuclear function in downregulating the activity of β-catenin. Using colorectal cell lines that express a mutant form of β-catenin, which cannot be phosphorylated by GSK-3β and ectopically expressed mutant β-catenin protein, we show that nuclear GSK-3β functions in a mechanism that does not involve β-catenin phosphorylation to reduce the levels of Wnt signalling. We show that GSK-3β enters the nucleus, forms a complex with β-catenin and lowers the levels of β-catenin/TCF-dependent transcription in a mechanism that involves GSK-3β–Axin binding.Oncogene (2008) 27, 3546–3555; doi:10.1038/sj.onc.1211026; published online 28 January 2008 [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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