Noncanonical Inflammasome Activation by Intracellular LPS Independent of TLR4

By N. Kayagaki, Michael Thomas Wong, Irma B. Stowe, S. R. Ramani, Lino C. Gonzalez, Sachiko Akashi-Takamura, K. Miyake, Juan Zhang, Wyne P. Lee, Artur Muszyński and 3 more. Science, 2013

1,456 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/7c28485e98826d2ef2cfd15867a1dca32bd92d39

How researchers see this paper

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

In Immunology

1. T. Kanneganti
2. M. Lamkanfi
3. S. Gordon
4. F. Martínez
5. Edward A. Miao
6. R. Malireddi
7. S. Kesavardhana
8. F. Shao

In Molecular Biology

1. T. Kanneganti
2. M. Lamkanfi
3. R. Malireddi
4. Edward A. Miao
5. S. Kesavardhana
6. S. Man
7. G. Núñez
8. Yuan He

In Pulmonary and Respiratory Medicine

1. S. Gordon
2. F. Martínez

Citations in the corpus

• GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death (2016, positive): “In contrast, the bacterial cell wall component lipopolysaccharide (LPS), one of the strongest immune-system activators, leads to the assembly of “non-canonical” inflammasomes through activation of caspase-4, caspase-5 or caspase-11 (Kayagaki et al , 2011, 2013; Hagar et al , 2013; Shi et al , 2014).”
• Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection (2018, background): “To trigger pyroptosis, LPS was transfected into the cytosol to activate caspase-11 (35).”
• Role of pyroptosis in inflammation and cancer (2022, background): “Furthermore, LPS is conducive to secreting and releasing a lectin called galectin-1 that can combine with β-galactoside, but the mechanism of secretion is still not well understood [42, 182, 183].”
• Bacterial outer membrane vesicles mediate cytosolic localization of LPS and caspase-11 activation (2016, positive): “Sensing of LPS in the cytosol by inflammatory caspases such as caspase-11 has emerged as a central mechanism of innate immune activation during Gram-negative bacterial infections as well as sepsis (Hagar et al., 2013; Kayagaki et al., 2013; Shi et al., 2014).”
• Caspases in cell death, inflammation and disease (2019, background): “In this pathway, internalized lipopolysaccharide (LPS) from Gram-negative bacteria interacts with the CARD domain and activates human caspases 4 and 5 and murine caspase-11 (Baker et al., 2015; Hagar et al., 2013; Kayagaki et al., 2013; Schmid-Burgk et al., 2015; Shi et al., 2014).”
• Pyroptotic cell death defends against intracellular pathogens (2015, background): “With the additional knowledge that LPS is the caspase-11 agonist, there are now two LPS detection pathways: cytosolic LPS is detected by caspase-11, and extracellular and vacuolar LPS is detected by TLR4, and Tlr4 / are also resistant to LPS-mediated endotoxic shock (89, 90, 107).”
• The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation (2019, background): “It was discovered that cytoplasmic LPS is sufficient for eliciting endotoxic shock independently of TLR4 signaling [121,122].”