MEKK2 mediates aberrant ERK activation in neurofibromatosis type I

Neurofibromatosis type I (NF1) is characterized by prominent skeletal abnormalities mediated in part by aberrant ERK pathway activation due to NF1 loss-of-function. Here, the authors report the MEKK2 is a key mediator of this aberrant ERK activation and that MEKK2 inhibitors, including ponatinib, am...

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Autores principales:	Seoyeon Bok, Dong Yeon Shin, Alisha R. Yallowitz, Mark Eiseman, Michelle Cung, Ren Xu, Na Li, Jun Sun, Alfred L. Williams, John E. Scott, Bing Su, Jae-Hyuck Shim, Matthew B. Greenblatt
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/1bdc5e8883dd407b82aab19c4cfb975b
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spelling	oai:doaj.org-article:1bdc5e8883dd407b82aab19c4cfb975b2021-12-02T14:40:41ZMEKK2 mediates aberrant ERK activation in neurofibromatosis type I10.1038/s41467-020-19555-62041-1723https://doaj.org/article/1bdc5e8883dd407b82aab19c4cfb975b2020-11-01T00:00:00Zhttps://doi.org/10.1038/s41467-020-19555-6https://doaj.org/toc/2041-1723Neurofibromatosis type I (NF1) is characterized by prominent skeletal abnormalities mediated in part by aberrant ERK pathway activation due to NF1 loss-of-function. Here, the authors report the MEKK2 is a key mediator of this aberrant ERK activation and that MEKK2 inhibitors, including ponatinib, ameliorate skeletal defects in a mouse model of NF1.Seoyeon BokDong Yeon ShinAlisha R. YallowitzMark EisemanMichelle CungRen XuNa LiJun SunAlfred L. WilliamsJohn E. ScottBing SuJae-Hyuck ShimMatthew B. GreenblattNature PortfolioarticleScienceQENNature Communications, Vol 11, Iss 1, Pp 1-10 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Seoyeon Bok Dong Yeon Shin Alisha R. Yallowitz Mark Eiseman Michelle Cung Ren Xu Na Li Jun Sun Alfred L. Williams John E. Scott Bing Su Jae-Hyuck Shim Matthew B. Greenblatt MEKK2 mediates aberrant ERK activation in neurofibromatosis type I
description	Neurofibromatosis type I (NF1) is characterized by prominent skeletal abnormalities mediated in part by aberrant ERK pathway activation due to NF1 loss-of-function. Here, the authors report the MEKK2 is a key mediator of this aberrant ERK activation and that MEKK2 inhibitors, including ponatinib, ameliorate skeletal defects in a mouse model of NF1.
format	article
author	Seoyeon Bok Dong Yeon Shin Alisha R. Yallowitz Mark Eiseman Michelle Cung Ren Xu Na Li Jun Sun Alfred L. Williams John E. Scott Bing Su Jae-Hyuck Shim Matthew B. Greenblatt
author_facet	Seoyeon Bok Dong Yeon Shin Alisha R. Yallowitz Mark Eiseman Michelle Cung Ren Xu Na Li Jun Sun Alfred L. Williams John E. Scott Bing Su Jae-Hyuck Shim Matthew B. Greenblatt
author_sort	Seoyeon Bok
title	MEKK2 mediates aberrant ERK activation in neurofibromatosis type I
title_short	MEKK2 mediates aberrant ERK activation in neurofibromatosis type I
title_full	MEKK2 mediates aberrant ERK activation in neurofibromatosis type I
title_fullStr	MEKK2 mediates aberrant ERK activation in neurofibromatosis type I
title_full_unstemmed	MEKK2 mediates aberrant ERK activation in neurofibromatosis type I
title_sort	mekk2 mediates aberrant erk activation in neurofibromatosis type i
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/1bdc5e8883dd407b82aab19c4cfb975b
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MEKK2 mediates aberrant ERK activation in neurofibromatosis type I

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