Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells

The c-MYC oncoprotein has many targets whose actions are not fully understood including TFAP4/AP4. Here, the authors show in a mouse model of inherited colorectal cancer that deletion of AP4 decreased the frequency of c-MYC-driven intestinal adenomas, and reveal Ap4 as a mediator of adenoma initiati...

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Autores principales:	Stephanie Jaeckel, Markus Kaller, Rene Jackstadt, Ursula Götz, Susanna Müller, Sophie Boos, David Horst, Peter Jung, Heiko Hermeking
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/c22477ac99a148f3b0a8d972d65afea8
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spelling	oai:doaj.org-article:c22477ac99a148f3b0a8d972d65afea82021-12-02T16:56:38ZAp4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells10.1038/s41467-018-06001-x2041-1723https://doaj.org/article/c22477ac99a148f3b0a8d972d65afea82018-09-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-06001-xhttps://doaj.org/toc/2041-1723The c-MYC oncoprotein has many targets whose actions are not fully understood including TFAP4/AP4. Here, the authors show in a mouse model of inherited colorectal cancer that deletion of AP4 decreased the frequency of c-MYC-driven intestinal adenomas, and reveal Ap4 as a mediator of adenoma initiation and regulator of colonic and intestinal stem cell and Paneth cell homeostasis.Stephanie JaeckelMarkus KallerRene JackstadtUrsula GötzSusanna MüllerSophie BoosDavid HorstPeter JungHeiko HermekingNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-17 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Stephanie Jaeckel Markus Kaller Rene Jackstadt Ursula Götz Susanna Müller Sophie Boos David Horst Peter Jung Heiko Hermeking Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells
description	The c-MYC oncoprotein has many targets whose actions are not fully understood including TFAP4/AP4. Here, the authors show in a mouse model of inherited colorectal cancer that deletion of AP4 decreased the frequency of c-MYC-driven intestinal adenomas, and reveal Ap4 as a mediator of adenoma initiation and regulator of colonic and intestinal stem cell and Paneth cell homeostasis.
format	article
author	Stephanie Jaeckel Markus Kaller Rene Jackstadt Ursula Götz Susanna Müller Sophie Boos David Horst Peter Jung Heiko Hermeking
author_facet	Stephanie Jaeckel Markus Kaller Rene Jackstadt Ursula Götz Susanna Müller Sophie Boos David Horst Peter Jung Heiko Hermeking
author_sort	Stephanie Jaeckel
title	Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells
title_short	Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells
title_full	Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells
title_fullStr	Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells
title_full_unstemmed	Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells
title_sort	ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/c22477ac99a148f3b0a8d972d65afea8
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Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells

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