Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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Evolution and Virulence of Influenza A Virus Protein PB1-F2.Trafficking of cholesterol to the ER is required for NLRP3 inflammasome activation

P2860

Q47246083-52A6337F-073E-4342-B1F4-D9A04A31B00D Q58793016-72C16B35-5C9E-4290-810C-B470AE8E98E0

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Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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http://www.wikidata.org/entity/Q47942982

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2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

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Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

@en

Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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P1476

Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses

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P2093

Takuma Misawa

http://www.w3.org/2001/XMLSchema#string

Tatsuya Saitoh

http://www.w3.org/2001/XMLSchema#string

P2860

Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

Mitochondrial DNA stress primes the antiviral innate immune response

Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle-Wells syndrome

Mitochondrial dynamics regulate the RIG-I-like receptor antiviral pathway

Chronic infantile neurological cutaneous and articular syndrome is caused by mutations in CIAS1, a gene highly expressed in polymorphonuclear cells and chondrocytes

NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder

De novo CIAS1 mutations, cytokine activation, and evidence for genetic heterogeneity in patients with neonatal-onset multisystem inflammatory disease (NOMID): a new member of the expanding family of pyrin-associated autoinflammatory diseases

The adaptor MAVS promotes NLRP3 mitochondrial localization and inflammasome activation

TRPM2 links oxidative stress to NLRP3 inflammasome activation

NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice

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187-197

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scholarly article

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10.1007/978-981-10-4567-7_14

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English

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997

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Michihiro Takahama

P577

2017-01-01T00:00:00Z

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P698

28815531

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P921

endoplasmic reticulum

Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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Mitochondria-Endoplasmic Reticulum Contact Sites Mediate Innate Immune Responses.

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P1433

P1476

P2093

P2860

P304

P31

P356

P407

P478

P50

P577

P698

P921

P356

P1433

P1476

P2093

P2860

P304

P31

P356

P407

P478

P50

P577

P698

P921