Influenza A virus protein PB1-F2 translocates into mitochondria via Tom40 channels and impairs innate immunity. (Q38964354)

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13 March 2020

title

Influenza A virus protein PB1-F2 translocates into mitochondria via Tom40 channels and impairs innate immunity (English)

1 reference

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13 March 2020

Influenza A virus

1 reference

7

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13 March 2020

author name string

Takuma Yoshizumi

1

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13 March 2020

Takeshi Ichinohe

2

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13 March 2020

Osamu Sasaki

3

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13 March 2020

Hidenori Otera

4

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13 March 2020

Shun-ichiro Kawabata

5

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13 March 2020

Katsuyoshi Mihara

6

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13 March 2020

language of work or name

English

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publication date

20 August 2014

1 reference

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13 March 2020

published in

Nature Communications

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13 March 2020

volume

5

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13 March 2020

page(s)

4713

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Biogenesis of mitochondria

13 March 2020

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Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-kappaB and IRF 3

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A role for mitochondria in NLRP3 inflammasome activation

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Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome

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Mitochondrial protein mitofusin 2 is required for NLRP3 inflammasome activation after RNA virus infection

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A novel influenza A virus mitochondrial protein that induces cell death.

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An insight into the PB1F2 protein and its multifunctional role in enhancing the pathogenicity of the influenza A viruses

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The influenza A virus PB1-F2 protein targets the inner mitochondrial membrane via a predicted basic amphipathic helix that disrupts mitochondrial function

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7 January 2021

Mitochondrial targeting sequence of the influenza A virus PB1-F2 protein and its function in mitochondria.

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7 January 2021

Influenza virus PB1-F2 protein induces cell death through mitochondrial ANT3 and VDAC1.

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Impact of amino acid mutations in PB2, PB1-F2, and NS1 on the replication and pathogenicity of pandemic (H1N1) 2009 influenza viruses

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A single mutation in the PB1-F2 of H5N1 (HK/97) and 1918 influenza A viruses contributes to increased virulence

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Export of mitochondrial AIF in response to proapoptotic stimuli depends on processing at the intermembrane space

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A novel insertion pathway of mitochondrial outer membrane proteins with multiple transmembrane segments.

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Regulation of mitochondrial morphology through proteolytic cleavage of OPA1

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7 January 2021

Stress-induced OMA1 activation and autocatalytic turnover regulate OPA1-dependent mitochondrial dynamics

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7 January 2021

Mitofusin 2 inhibits mitochondrial antiviral signaling

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7 January 2021

Influenza virus protein PB1-F2 inhibits the induction of type I interferon by binding to MAVS and decreasing mitochondrial membrane potential

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7 January 2021

The adaptor MAVS promotes NLRP3 mitochondrial localization and inflammasome activation

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7 January 2021

Activation and regulation of the inflammasomes

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Hepatitis C virus protease NS3/4A cleaves mitochondrial antiviral signaling protein off the mitochondria to evade innate immunity

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Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus

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7 January 2021

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7 January 2021

Expression of the 1918 influenza A virus PB1-F2 enhances the pathogenesis of viral and secondary bacterial pneumonia

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7 January 2021

Naturally occurring swine influenza A virus PB1-F2 phenotypes that contribute to superinfection with Gram-positive respiratory pathogens

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7 January 2021

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7 January 2021

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Identifiers

DOI

10.1038/NCOMMS5713

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:25140902%20AND%20SRC:MED&resulttype=core&format=json

Dimensions Publication ID

13 March 2020

ADS bibcode

2014NatCo...5.4713Y

0 references

1008587013

0 references

Fatcat ID

release_ermit5pv7jfbvdpyzrcp6llope

1 reference

Fatcat

https://api.fatcat.wiki/v0/release/ermit5pv7jfbvdpyzrcp6llope

24 November 2022

mapped directly with Wikidata item

1 reference