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  1. 原著論文

NEK9 regulates primary cilia formation by acting as a selective autophagy adaptor for MYH9/myosin IIA.

https://repo.qst.go.jp/records/82940
https://repo.qst.go.jp/records/82940
9606da5f-28ff-4b89-808e-785a3b6ef104
Item type 学術雑誌論文 / Journal Article(1)
公開日 2021-06-04
タイトル
タイトル NEK9 regulates primary cilia formation by acting as a selective autophagy adaptor for MYH9/myosin IIA.
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Yamamoto, Yasuhiro

× Yamamoto, Yasuhiro

WEKO 996749

Yamamoto, Yasuhiro

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Chino, Haruka

× Chino, Haruka

WEKO 996750

Chino, Haruka

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Tsukamoto, Satoshi

× Tsukamoto, Satoshi

WEKO 996751

Tsukamoto, Satoshi

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L Ode, Koji

× L Ode, Koji

WEKO 996752

L Ode, Koji

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R Ueda, Hiroki

× R Ueda, Hiroki

WEKO 996753

R Ueda, Hiroki

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Mizushima, Noboru

× Mizushima, Noboru

WEKO 996754

Mizushima, Noboru

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Satoshi, Tsukamoto

× Satoshi, Tsukamoto

WEKO 996755

en Satoshi, Tsukamoto

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抄録
内容記述タイプ Abstract
内容記述 Autophagy regulates primary cilia formation, but the underlying mechanism is not fully understood. In this study, we identify NIMA-related kinase 9 (NEK9) as a GABARAPs-interacting protein and find that NEK9 and its LC3-interacting region (LIR) are required for primary cilia formation. Mutation in the LIR of NEK9 in mice also impairs in vivo cilia formation in the kidneys. Mechanistically, NEK9 interacts with MYH9 (also known as myosin IIA), which has been implicated in inhibiting ciliogenesis through stabilization of the actin network. MYH9 accumulates in NEK9 LIR mutant cells and mice, and depletion of MYH9 restores ciliogenesis in NEK9 LIR mutant cells. These results suggest that NEK9 regulates ciliogenesis by acting as an autophagy adaptor for MYH9. Given that the LIR in NEK9 is conserved only in land vertebrates, the acquisition of the autophagic regulation of the NEK9-MYH9 axis in ciliogenesis may have possible adaptive implications for terrestrial life.
書誌情報 Nature Communications

巻 12, 号 1, p. 3292-1, 発行日 2021-06
出版者
出版者 Nature
ISSN
収録物識別子タイプ ISSN
収録物識別子 2041-1723
PubMed番号
識別子タイプ PMID
関連識別子 34078910
DOI
識別子タイプ DOI
関連識別子 10.1038/s41467-021-23599-7
関連サイト
識別子タイプ URI
関連識別子 https://www.nature.com/articles/s41467-021-23599-7
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