Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin

By Eric D. Boyden, W. Dietrich. Nature Genetics, 2006

866 citations recorded by the source corpus.

Subfields: Genetics, Infectious Diseases, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/5501369cf0ab685f983b2f2f11d6bab410636790

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. J. Tschopp
2. G. Núñez
3. M. Lamkanfi
4. V. Dixit
5. Taro Kawai
6. Fabio Martinon
7. L. Franchi
8. T. Kanneganti

In Infectious Diseases

1. Shizuo Akira
2. J. Tschopp
3. Taro Kawai
4. G. Núñez
5. M. Lamkanfi
6. V. Dixit
7. Fabio Martinon
8. L. Franchi

In Molecular Biology

1. T. Kanneganti
2. J. Tschopp
3. M. Lamkanfi
4. G. Núñez
5. Shizuo Akira
6. V. Dixit
7. S. Man
8. Taro Kawai

Citations in the corpus

• Pyroptotic cell death defends against intracellular pathogens (2015, background): “Like PYD-containing proteins, it remains unclear if CrmA and other SPI proteins inhibit pyroptosis besides preventing cytokine production.”
• The inflammasomes: guardians of the body. (2009, background): “This trait difference has been mapped to a locus on chromosome 11 and is associated with a polymorphism in the nalp1b gene that impinges on caspase-1 activation (175).”
• Inflammatory caspases and inflammasomes: master switches of inflammation (2007, background): “named Ltxs1, and was recently associated with NALP1b gene.(99) The NALP1 locus in mouse contains three paralogues, NALP1a, NALP1b and NALP1c (Table 1).”
• Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death. (2017, background): “This caused confusions in understanding LT-induced death before the identification of Nlrp1b as the determinant for macrophage susceptibility to LT-induced caspase-1-dependent death [68].”
• Caspase-1 induced pyroptotic cell death (2011, background): “NLRC4 responds to cytosolic flagellin or T3SS rod proteins (16, 19), murine NLRP1b responds to anthrax lethal toxin (20), AIM2 responds to cytosolic DNA (18), and NLRP3 responds to a variety of agonists including crystals (17).”
• The inflammasomes. (2010, neutral): “Strain variation in the mouse Nlrp1b locus appears to underlie susceptibility to Bacillus anthracis lethal toxin (LeTx), as macrophages from susceptible, but not resistant, mouse strains activate caspase-1 after LeTx exposure (Boyden and Dietrich, 2006).”
• Glyburide inhibits the Cryopyrin/Nalp3 inflammasome (2009, background): “The SUR subunits belong to the ATP-binding cassette (ABC) transporter family (Aguilar-Bryan et al., 1995) and function as a regulatory subunit, endowing the Kir6.x channel with sensitivity to inhibition by sulfonylureas such as glyburide and glipizide (Ashcroft, 2005).”
• Nod-like proteins in immunity, inflammation and disease (2006, background): “Mice carrying an allele of Nalp1 encoding the protein NALP1b are susceptible to the effects of lethal toxin of Bacillus anthracis”
• Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? (2015, neutral): “Extensive studies in macrophages and in reconstituted systems have demonstrated that NLRP1 is sensitive to both bacterial cell wall component muramyl dipeptide (MDP) and Bacillus anthracis lethal toxin (19, 38).”
• Understanding the mechanism of IL-1β secretion (2011, neutral): “lethal toxin [30].”
• The Inflammasome: A Caspase-1 Activation Platform Regulating Immune Responses and Disease Pathogenesis (2009, background): “Genetic studies have identified Nlrp1b as the gene that encodes the molecule responsible for the pathology induced by lethal toxin, secreted by Bacillus anthracis”