Pannexin‐1 mediates large pore formation and interleukin‐1β release by the ATP‐gated P2X7 receptor
By P. Pelegrín, A. Surprenant. EMBO Journal, 2006
1,479 citations recorded by the source corpus.
Subfields: Endocrine and Autonomic Systems, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/95cf9250c97d9a7edb497cb5baa40f0ed73e7345
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In Endocrine and Autonomic Systems
In Molecular Biology
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Citations in the corpus
- Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? (2015, background): “For example, excessive levels of ATP were described as one of the first endogenous DAMPs to induce NLRP3 inflammasome formation and activation, a mechanism involving high concentrations of extracellular ATP binding to the purinergic P2X7 receptor (104).”
- The Inflammasome: A Caspase-1 Activation Platform Regulating Immune Responses and Disease Pathogenesis (2009, background): “Evidence indicates that extracellular ATP also results in the opening of a pore mediated by pannexin-1 (refs”
- The Family of Connexin Genes (2009, background): “While pannexins can form channels connecting the cytoplasm and extracellular space analogous to connexin hemichannels [11,12, 13 ], it is not clear that they form intercellular channels except in certain overexpression systems [11,14,15] (see Chapter 12).”
- Function of Nod‐like receptors in microbial recognition and host defense (2009, background): “Pelegrin P, Surprenant A. Pannexin-1 medi- ates large pore formation and interleukin1beta release by the ATP-gated P2X7 receptor.”
- The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation (2019, background): “Caspases-4/5/11 induce pyroptosis through the processing of GSDMD, and pannexin-1, which is a protein channel that releases ATP from the cell [17,71,128].”
- NLRP3 inflammasome activation: the convergence of multiple signalling pathways on ROS production? (2010, background): “Although the mechanism by which cytoplasmic K + concentration modulates NLRP3 inflammasome activation is unknown, it seems that intracellular K + depletion alone is not sufficient for NLRP3-mediated IL-1β processing and secretio”