Fatty acid–induced NLRP3-ASC inflammasome activation interferes with insulin signaling
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Title
Fatty acid–induced NLRP3-ASC inflammasome activation interferes with insulin signaling
Authors
Keywords
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Journal
NATURE IMMUNOLOGY
Volume 12, Issue 5, Pages 408-415
Publisher
Springer Nature
Online
2011-04-11
DOI
10.1038/ni.2022
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Note: Only part of the references are listed.- Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
- (2014) Daniel J. Klionsky et al. Autophagy
- Autophagy in immunity and inflammation
- (2011) Beth Levine et al. NATURE
- AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1
- (2011) Joungmok Kim et al. NATURE CELL BIOLOGY
- The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance
- (2011) Bolormaa Vandanmagsar et al. NATURE MEDICINE
- The Inflammasomes
- (2010) Kate Schroder et al. CELL
- Defective Hepatic Autophagy in Obesity Promotes ER Stress and Causes Insulin Resistance
- (2010) Ling Yang et al. Cell Metabolism
- AMPKα2 Deletion Causes Aberrant Expression and Activation of NAD(P)H Oxidase and Consequent Endothelial Dysfunction In Vivo
- (2010) Shuangxi Wang et al. CIRCULATION RESEARCH
- Macrophage α1 AMP-activated Protein Kinase (α1AMPK) Antagonizes Fatty Acid-induced Inflammation through SIRT1
- (2010) Zhenggang Yang et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- A role for mitochondria in NLRP3 inflammasome activation
- (2010) Rongbin Zhou et al. NATURE
- The AIM2 inflammasome is critical for innate immunity to Francisella tularensis
- (2010) Teresa Fernandes-Alnemri et al. NATURE IMMUNOLOGY
- Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome
- (2010) Kiichi Nakahira et al. NATURE IMMUNOLOGY
- Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes
- (2010) Seth L Masters et al. NATURE IMMUNOLOGY
- Blockade of interleukin 1 in type 1 diabetes mellitus
- (2010) Thomas Mandrup-Poulsen et al. Nature Reviews Endocrinology
- How the Noninflammasome NLRs Function in the Innate Immune System
- (2010) J. P. Y. Ting et al. SCIENCE
- Phosphorylation of ULK1 (hATG1) by AMP-Activated Protein Kinase Connects Energy Sensing to Mitophagy
- (2010) D. F. Egan et al. SCIENCE
- Lipid Droplets Finally Get a Little R-E-S-P-E-C-T
- (2009) Robert V. Farese et al. CELL
- As a Matter of Fat
- (2009) Rita T. Brookheart et al. Cell Metabolism
- Cutting Edge: NF- B Activating Pattern Recognition and Cytokine Receptors License NLRP3 Inflammasome Activation by Regulating NLRP3 Expression
- (2009) F. G. Bauernfeind et al. JOURNAL OF IMMUNOLOGY
- Thioredoxin-interacting protein links oxidative stress to inflammasome activation
- (2009) Rongbin Zhou et al. NATURE IMMUNOLOGY
- Islet G protein-coupled receptors as potential targets for treatment of type 2 diabetes
- (2009) Bo Ahrén NATURE REVIEWS DRUG DISCOVERY
- AMPK in Health and Disease
- (2009) Gregory R. Steinberg et al. PHYSIOLOGICAL REVIEWS
- The NLR Gene Family: A Standard Nomenclature
- (2008) Jenny P.-Y. Ting et al. IMMUNITY
- Crucial role for the Nalp3 inflammasome in the immunostimulatory properties of aluminium adjuvants
- (2008) Stephanie C. Eisenbarth et al. NATURE
- Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production
- (2008) Tatsuya Saitoh et al. NATURE
- Fatty acid-binding proteins: role in metabolic diseases and potential as drug targets
- (2008) Masato Furuhashi et al. NATURE REVIEWS DRUG DISCOVERY
- A Stress Signaling Pathway in Adipose Tissue Regulates Hepatic Insulin Resistance
- (2008) G. Sabio et al. SCIENCE
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