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Adenomatous polyposis coli
From Proteopedia
(Difference between revisions)
(New page: ==Adenomatous polyposis coli== <StructureSection load='1stp' size='340' side='right' caption='Caption for this structure' scene=''> '''Adenomatous polyposis coli (APC)''' is a multidomain ...) |
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==Adenomatous polyposis coli== | ==Adenomatous polyposis coli== | ||
<StructureSection load='1stp' size='340' side='right' caption='Caption for this structure' scene=''> | <StructureSection load='1stp' size='340' side='right' caption='Caption for this structure' scene=''> | ||
| - | '''Adenomatous polyposis coli (APC)''' is a multidomain tumour suppressor protein involved in the regulation of various cellular processes, such as cell adhesion, migration or proliferation<ref name="Zhang2017">Zhang, L. and Shay, J. W. (2017) ‘Multiple Roles of APC and its Therapeutic Implications in Colorectal Cancer.’, Journal of the National Cancer Institute, 109(8). doi: 10.1093/jnci/djw332.</ref>. It is expressed in plethora of organs and tissues, e. g. cerebral cortex, bronchi or the gastrointestinal tract<ref name="proteinatlas">https://www.proteinatlas.org/ENSG00000134982-APC/tissue</ref>. Germline truncation mutations of APC result in familial adenomatous polyposis, a hereditary form of colon cancer<ref name="Ficari2000">Ficari, F. et al. (2000) ‘APC gene mutations and colorectal adenomatosis in familial adenomatous polyposis’, British Journal of Cancer. Churchill Livingstone, 82(2), pp. 348–353. doi: 10.1054/bjoc.1999.0925.</ref>. Additionally, loss of the C-terminal portion of APC is detected in about 80 % of sporadic colon cancers<ref name="Rowan2000">Rowan, A. J. et al. (2000) ‘APC mutations in sporadic colorectal tumors: A mutational “hotspot” and interdependence of the “two hits”’, Proceedings of the National Academy of Sciences of the United States of America. National Academy of Sciences, 97(7), pp. 3352–3357. doi: 10.1073/pnas.97.7.3352.</ref>. | + | '''<scene name='84/843011/Pokus1/1'>Adenomatous polyposis coli (APC)</scene>''' is a multidomain tumour suppressor protein involved in the regulation of various cellular processes, such as cell adhesion, migration or proliferation<ref name="Zhang2017">Zhang, L. and Shay, J. W. (2017) ‘Multiple Roles of APC and its Therapeutic Implications in Colorectal Cancer.’, Journal of the National Cancer Institute, 109(8). doi: 10.1093/jnci/djw332.</ref>. It is expressed in plethora of organs and tissues, e. g. cerebral cortex, bronchi or the gastrointestinal tract<ref name="proteinatlas">https://www.proteinatlas.org/ENSG00000134982-APC/tissue</ref>. Germline truncation mutations of APC result in familial adenomatous polyposis, a hereditary form of colon cancer<ref name="Ficari2000">Ficari, F. et al. (2000) ‘APC gene mutations and colorectal adenomatosis in familial adenomatous polyposis’, British Journal of Cancer. Churchill Livingstone, 82(2), pp. 348–353. doi: 10.1054/bjoc.1999.0925.</ref>. Additionally, loss of the C-terminal portion of APC is detected in about 80 % of sporadic colon cancers<ref name="Rowan2000">Rowan, A. J. et al. (2000) ‘APC mutations in sporadic colorectal tumors: A mutational “hotspot” and interdependence of the “two hits”’, Proceedings of the National Academy of Sciences of the United States of America. National Academy of Sciences, 97(7), pp. 3352–3357. doi: 10.1073/pnas.97.7.3352.</ref>. |
== Function == | == Function == | ||
Revision as of 20:07, 28 April 2020
Adenomatous polyposis coli
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References
- ↑ Zhang, L. and Shay, J. W. (2017) ‘Multiple Roles of APC and its Therapeutic Implications in Colorectal Cancer.’, Journal of the National Cancer Institute, 109(8). doi: 10.1093/jnci/djw332.
- ↑ https://www.proteinatlas.org/ENSG00000134982-APC/tissue
- ↑ Ficari, F. et al. (2000) ‘APC gene mutations and colorectal adenomatosis in familial adenomatous polyposis’, British Journal of Cancer. Churchill Livingstone, 82(2), pp. 348–353. doi: 10.1054/bjoc.1999.0925.
- ↑ Rowan, A. J. et al. (2000) ‘APC mutations in sporadic colorectal tumors: A mutational “hotspot” and interdependence of the “two hits”’, Proceedings of the National Academy of Sciences of the United States of America. National Academy of Sciences, 97(7), pp. 3352–3357. doi: 10.1073/pnas.97.7.3352.
