ATP translocates from cytosol to extracellular space (stimuated by C3AR1:C3a)

Stable Identifier
Reaction [BlackBoxEvent]
Homo sapiens
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It has been shown that anaphylatoxin C3a binding to its receptor C3AR1 indirectly activates the proinflammatory cytokine IL1β (Laudisi, 2013 and Asgari, 2013). Asgari et al. suggest a mechanism; after the binding of C3a to C3AR1, ATP release is promoted from the cytosol to the extracellular space through an unknown channel. From here, ATP binding to P2X purinoceptors activates the inflammasome that results in the production of IL1β (Asgari 2013).

Literature References
PubMed ID Title Journal Year
23817414 Cutting edge: the NLRP3 inflammasome links complement-mediated inflammation and IL-1β release

Morgan, BP, Evrard, M, Sivasankar, B, Laudisi, F, Hughes, TR, Mandriani, B, Spreafico, R, Mortellaro, A, Kandasamy, M

J. Immunol. 2013
23878142 C3a modulates IL-1β secretion in human monocytes by regulating ATP efflux and subsequent NLRP3 inflammasome activation

Sacks, SS, Cook, HT, Le Friec, G, Asgari, E, Kemper, C, Yamamoto, H, Perucha, E, Köhl, J

Blood 2013
This event is regulated
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