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Nuclear export of the APC tumour suppressor controls β-catenin function in transcription

The adenomatous polyposis coli (APC) protein is inactivated in most colorectal tumours. APC loss is an early event in tumorigenesis, and causes an increase of nuclear β-catenin and its transcriptional activity. This is thought to be the driving force for tumour progression. APC shuttles in and out o...

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Detaylı Bibliyografya
Asıl Yazarlar: Rosin-Arbesfeld, Rina, Cliffe, Adam, Brabletz, Thomas, Bienz, Mariann
Materyal Türü: Artigo
Dil:Inglês
Baskı/Yayın Bilgisi: Oxford University Press 2003
Konular:
Online Erişim:https://ncbi.nlm.nih.gov/pmc/articles/PMC150338/
https://ncbi.nlm.nih.gov/pubmed/12606575
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/emboj/cdg105
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