NS1-binding protein abrogates the elevation of cell viability by the influenza A virus NS1 protein in association with CRKL

Miyazaki, Masaya; Nishihara, Hiroshi; Hasegawa, Hideki; Tashiro, Masato; Wang, Lei; Kimura, Taichi; Tanino, Mishie; Tsuda, Masumi; Tanaka, Shinya

NS1-binding protein abrogates the elevation of cell viability by the influenza A virus NS1 protein in association with CRKL

Miyazaki, Masaya; Nishihara, Hiroshi; Hasegawa, Hideki et al.

Biochemical and biophysical research communications, 2013, 441(4), 953-957

Permalink : https://hdl.handle.net/2115/54561

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アクセス権	open access
URI	https://hdl.handle.net/2115/54561
タイトル	NS1-binding protein abrogates the elevation of cell viability by the influenza A virus NS1 protein in association with CRKL
著者	Miyazaki, Masaya ; Nishihara, Hiroshi ; Hasegawa, Hideki ; Tashiro, Masato ; Wang, Lei ; Kimura, Taichi ; Tanino, Mishie ; Tsuda, Masumi ; Tanaka, Shinya
著者名 Miyazaki, Masaya
e-Rad_Researcher 50322805 著者名 Nishihara, Hiroshi
著者名 Hasegawa, Hideki
著者名 Tashiro, Masato
著者名 Wang, Lei
e-Rad_Researcher 90435959 著者名 Kimura, Taichi
e-Rad_Researcher 90360908 著者名 Tanino, Mishie
e-Rad_Researcher 30431307 著者名 Tsuda, Masumi
e-Rad_Researcher 70261287 著者名 Tanaka, Shinya
言語	英語
キーワード	NS1
	CrkL
	CrkII
	NS1-BP
	Cell proliferation
	ERK
発行日	2013-11-29
出版者	Academic press inc elsevier science
収録物名	Biochemical and biophysical research communications
巻(号)	441(4)
ページ	953-957
抄録	The influenza A virus non-structural protein 1 (NS1) is a multifunctional virulence factor consisting of an RNA binding domain and several Src-homology (SH) 2 and SH3 binding motifs, which promotes virus replication in the host cell and helps to evade antiviral immunity. NS1 modulates general host cell physiology in association with various cellular molecules including NS1-binding protein (NS1-BP) and signaling adapter protein CRK-like (CRKL), while the physiological role of NS1-BP during influenza A virus infection especially in association with NS1 remains unclear. In this study, we analyzed the intracellular association of NS1-BP, NS1 and CRKL to elucidate the physiological roles of these molecules in the host cell. In HEK293T cells, enforced expression of NS1 of A/Beijing (H1N1) and A/Indonesia (H5N1) significantly induced excessive phosphorylation of ERR and elevated cell viability, while the over-expression of NS1-BP and the abrogation of CRKL using siRNA abolished such survival effect of NS1. The pull-down assay using GST-fusion CRKL revealed the formation of intracellular complexes of NS1-BP, NS1 and CRKL. In addition, we identified that the N-terminus SH3 domain of CRKL was essential for binding to NS1-BP using GST-fusion CRKL-truncate mutants. This is the first report to elucidate the novel function of NS1-BP collaborating with viral protein NS1 in modulation of host cell physiology. In addition, an alternative role of adaptor protein CRKL in association with NS1 and NS1-BP during influenza A virus infection is demonstrated. (C) 2013 Elsevier Inc. All rights reserved.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
PISSN	0006-291X
NCID	AA00564395
関連情報	PMID 24220336
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1016/j.bbrc.2013.11.011