Author response for "Acetylation of the influenza A virus polymerase subunit PA in the N-terminal domain positively regulates its endonuclease activity"

Hatakeyama, Dai; Shoji, Masaki; Ogata, Seiryo; Masuda, Takeshi; Nakano, Masahiro; Komatsu, Tsugunori; Saitoh, Ayaka; Makiyama, Kyoko; Tsuneishi, Hazuki; Miyatake, Asuka; Takahira, Mizuki; Nishikawa, Erina; Ohkubo, Ayana; Noda, Takeshi; Kawaoka, Yoshihiro; Ohtsuki, Sumio; Kuzuhara, Takashi

doi:10.1111/febs.16123/v2/response1

2021

DOI: 10.1111/febs.16123/v2/response1

|View full text |Cite

Author response for "Acetylation of the influenza A virus polymerase subunit PA in the N-terminal domain positively regulates its endonuclease activity"

Dai Hatakeyama¹,

Masaki Shoji²,

Seiryo Ogata³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2022

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Human N-Alpha-Acetyltransferase 60 Promotes Influenza A Virus Infection by Dampening the Interferon Alpha Signaling

Ahmed

Husain

2022

Front. Immunol.

View full text Add to dashboard Cite

N-alpha-acetyltransferase 60 (NAA60) is the most recently discovered N-terminal acetyltransferase and found only in multicellular eukaryotes. NAA60 localizes to the Golgi complex and is one of the only two N-terminal acetyltransferases known to localize to an organelle. Furthermore, NAA60 possesses a unique ability of catalyzing the acetylation of membrane-anchored proteins at the N-terminus and histones at the lysine side chains. Herein, we demonstrate that NAA60 exhibits proviral properties during influenza A virus (IAV) infection by interfering with the interferon (IFN) α signaling. We found that the depletion and overexpression of NAA60 reduced and enhanced, respectively, the IAV growth in a cell type- and IAV strain-independent manner. Mechanistically, the IAV-induced expression of IFNα was increased and decreased in NAA60-depleted and -overexpressing cells, respectively. Furthermore, the depletion of NAA60 enhanced the level of phosphorylated STAT1 transcription factor as well as the expression of several IFN-stimulated genes (ISGs) such as MX1, CH25H, IFITM3, ISG15 and viperin in infected cells. Whereas the overexpression of NAA60 produced opposite results. Finally, similar results were obtained when the NAA60-depleted cells were treated with purified IFNα. These findings, in conjunction with our recent findings where N-terminal acetylation of many host proteins increased in response to the IAV infection, indicate an important role of N-terminal acetylation during IAV replication.

show abstract

Human N-Alpha-Acetyltransferase 60 Promotes Influenza A Virus Infection by Dampening the Interferon Alpha Signaling

Ahmed

Husain

2022

Front. Immunol.

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Author response for "Acetylation of the influenza A virus polymerase subunit PA in the N-terminal domain positively regulates its endonuclease activity"

Cited by 1 publication

References 0 publications

Human N-Alpha-Acetyltransferase 60 Promotes Influenza A Virus Infection by Dampening the Interferon Alpha Signaling

Human N-Alpha-Acetyltransferase 60 Promotes Influenza A Virus Infection by Dampening the Interferon Alpha Signaling

Contact Info

Product

Resources

About