Mitochondrial apoptosis is dispensable for NLRP 3 inflammasome activation but non‐apoptotic caspase‐8 is required for inflammasome priming-Reference-Cited by-全球学者库

Mitochondrial apoptosis is dispensable for NLRP 3 inflammasome activation but non‐apoptotic caspase‐8 is required for inflammasome priming

Published:2014-07-02 Issue:9 Volume:15 Page:982-990
ISSN:1469-221X
Container-title:EMBO reports
language:en
Short-container-title:EMBO Rep

Author:

Allam Ramanjaneyulu¹,Lawlor Kate E²³,Yu Eric Chi‐Wang¹,Mildenhall Alison L²³,Moujalled Donia M²³,Lewis Rowena S²³,Ke Francine²³,Mason Kylie D²³,White Michael J²³,Stacey Katryn J⁴,Strasser Andreas²³,O'Reilly Lorraine A²³,Alexander Warren²³,Kile Benjamin T²³,Vaux David L²³,Vince James E²³

Affiliation:

1. Department of Biochemistry University of Lausanne Epalinges Switzerland

2. The Walter and Eliza Hall Institute of Medical Research Parkville Victoria Australia

3. Department of Medical Biology The University of Melbourne Parkville Victoria Australia

4. School of Chemistry and Molecular Biosciences The University of Queensland Brisbane Qld Australia

Publisher

EMBO

Subject

Genetics,Molecular Biology,Biochemistry

Link

https://onlinelibrary.wiley.com/doi/pdf/10.15252/embr.201438463

Reference35 articles.

1. Pyroptotic death storms and cytopenia

2. More to life than death: molecular determinants of necroptotic and non-necroptotic RIP3 kinase signaling

3. Ambiguities in NLRP3 inflammasome regulation: Is there a role for mitochondria?

4. Oxidized Mitochondrial DNA Activates the NLRP3 Inflammasome during Apoptosis

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

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