ArticleInfection and immunity2013
Activation of the Nlrp1b inflammasome by reduction of cytosolic ATP.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed.
- Unmasking programmed cell death in rhinovirus-driven asthma pathology.Biochemical Society transactions · 2026Review
- When Infection Meets Inflammation:Biology · 2026Review
- Targeting innate immune sensors for therapeutic strategies in infectious diseases.Journal of microbiology (Seoul, Korea) · 2025Review
- Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection.Neurobiology of sleep and circadian rhythms · 2025Article
- Pattern Recognition by NOD-Like Receptors.Advances in experimental medicine and biology · 2025Review
- Inflammasomes and their role in PANoptosomes.Current opinion in immunology · 2024Review
- Activation of the NLRP1B inflammasome by caspase-8.Communications biology · 2024Article
- Article
- NLRP inflammasomes in health and disease.Molecular biomedicine · 2024Review
- The interaction of inflammasomes and gut microbiota: novel therapeutic insights.Cell communication and signaling : CCS · 2024Review
- Involution of brown adipose tissue through a Syntaxin 4 dependent pyroptosis pathway.Nature communications · 2024Article
- Interleukin-1beta and inflammasome expression in spinal cord following chronic constriction injury in male and female rats.Brain, behavior, and immunity · 2024Article
- The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023Review
- Why Is Iron Deficiency/Anemia Linked to Alzheimer's Disease and Its Comorbidities, and How Is It Prevented?Biomedicines · 2023Review
- Reductive cell death: the other side of the coin.Cancer gene therapy · 2023Article
- P38 kinases mediate NLRP1 inflammasome activation after ribotoxic stress response and virus infection.The Journal of experimental medicine · 2023Article
- Benzo[Frontiers in immunology · 2023Article
- Emerging mechanisms and functions of inflammasome complexes in teleost fish.Frontiers in immunology · 2023Review
- Oxidized thioredoxin-1 restrains the NLRP1 inflammasome.Science immunology · 2022Article
- Activation and Pharmacological Regulation of Inflammasomes.Biomolecules · 2022Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors.
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Abstract
The efficacy of the innate immune system depends on its ability to mount an appropriate response to diverse infections and damaging agents. Key components of this system are pattern recognition receptors that detect pathogen-associated and damage-associated molecular patterns (PAMPs and DAMPs). Nlrp1b is a pattern recognition receptor that forms a caspase-1 activation platform, known as an inflammasome, upon sensing the proteolytic activity of anthrax lethal toxin. The activation of caspase-1 leads to the release of proinflammatory cytokines that aid in the clearance of the anthrax infection. Here, we demonstrate that Nlrp1b also becomes activated in cells that are subjected to energy stress caused by metabolic inhibitors or by nutrient deprivation. Glucose starvation and hypoxia were used to correlate the level of cytosolic ATP to the degree of inflammasome activation. Because lowering the ratio of cytosolic ATP to AMP activates the main cellular energy sensor, AMP-activated protein kinase (AMPK), we assessed whether AMPK promoted inflammasome activity by using a combination of small interfering RNA (siRNA) and transfection of a dominant negative AMPK subunit. We found that AMPK promoted inflammasome activity, but activation of AMPK in the absence of ATP depletion was not sufficient for caspase-1-mediated pro-interleukin 1β (pro-IL-1β) processing. Finally, we found that mutation of the ATP-binding motif of Nlrp1b caused constitutive activation, suggesting that ATP might inhibit the Nlrp1b inflammasome instead of being required for its assembly.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.