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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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| Autors principals: | , , , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
Oxford University Press
2003
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| Matèries: | |
| Accés en línia: | 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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