Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology

Progranulin (PGRN) mutations cause frontotemporal lobe dementia with TDP-43 pathology. Here the authors develop a mutant PGRN knock-in mouse model of the disease, and show that Tyro3, a tyrosine kinase membrane receptor that acts upstream of PKC and MAPK, is inhibited by PGRN which contributes to pa...

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Autores principales: Kyota Fujita, Xigui Chen, Hidenori Homma, Kazuhiko Tagawa, Mutsuki Amano, Ayumu Saito, Seiya Imoto, Hiroyasu Akatsu, Yoshio Hashizume, Kozo Kaibuchi, Satoru Miyano, Hitoshi Okazawa
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Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/09ed0cd6cc5041bf8759b3550eb3f80b
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spelling oai:doaj.org-article:09ed0cd6cc5041bf8759b3550eb3f80b2021-12-02T14:39:23ZTargeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology10.1038/s41467-018-02821-z2041-1723https://doaj.org/article/09ed0cd6cc5041bf8759b3550eb3f80b2018-01-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-02821-zhttps://doaj.org/toc/2041-1723Progranulin (PGRN) mutations cause frontotemporal lobe dementia with TDP-43 pathology. Here the authors develop a mutant PGRN knock-in mouse model of the disease, and show that Tyro3, a tyrosine kinase membrane receptor that acts upstream of PKC and MAPK, is inhibited by PGRN which contributes to pathology in this model.Kyota FujitaXigui ChenHidenori HommaKazuhiko TagawaMutsuki AmanoAyumu SaitoSeiya ImotoHiroyasu AkatsuYoshio HashizumeKozo KaibuchiSatoru MiyanoHitoshi OkazawaNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-21 (2018)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Kyota Fujita
Xigui Chen
Hidenori Homma
Kazuhiko Tagawa
Mutsuki Amano
Ayumu Saito
Seiya Imoto
Hiroyasu Akatsu
Yoshio Hashizume
Kozo Kaibuchi
Satoru Miyano
Hitoshi Okazawa
Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology
description Progranulin (PGRN) mutations cause frontotemporal lobe dementia with TDP-43 pathology. Here the authors develop a mutant PGRN knock-in mouse model of the disease, and show that Tyro3, a tyrosine kinase membrane receptor that acts upstream of PKC and MAPK, is inhibited by PGRN which contributes to pathology in this model.
format article
author Kyota Fujita
Xigui Chen
Hidenori Homma
Kazuhiko Tagawa
Mutsuki Amano
Ayumu Saito
Seiya Imoto
Hiroyasu Akatsu
Yoshio Hashizume
Kozo Kaibuchi
Satoru Miyano
Hitoshi Okazawa
author_facet Kyota Fujita
Xigui Chen
Hidenori Homma
Kazuhiko Tagawa
Mutsuki Amano
Ayumu Saito
Seiya Imoto
Hiroyasu Akatsu
Yoshio Hashizume
Kozo Kaibuchi
Satoru Miyano
Hitoshi Okazawa
author_sort Kyota Fujita
title Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology
title_short Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology
title_full Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology
title_fullStr Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology
title_full_unstemmed Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology
title_sort targeting tyro3 ameliorates a model of pgrn-mutant ftld-tdp via tau-mediated synaptic pathology
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/09ed0cd6cc5041bf8759b3550eb3f80b
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