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Fig. 7 | Cell Communication and Signaling

Fig. 7

From: F0F1 ATP synthase regulates extracellular calcium influx in human neutrophils by interacting with Cav2.3 and modulates neutrophil accumulation in the lipopolysaccharide-challenged lung

Fig. 7

Proposed mechanism of cell surface F-ATPase-mediated regulation of Ca2+ influx. Stimulation with FPR triggers glycolysis to generate bulk intracellular protons and ATP that can be exported via F-ATPase, the pan1 channel, etc. Subsequently, ATP is hydrolyzed by CD39 to generate ADP and inorganic phosphate, which can be used to regenerate extracellular ATP with intracellular protons exported by F-ATPase to prolong cell surface ATP signaling and promote intracellular alkalization. The produced ATP indirectly regulates the P2 receptor to regulate Ca2+ influx. In addition, F-ATPase itself will affect Ca2+ influx by interacting with Cav2.3. Calcium influx plays a key role in ERK1/2 phosphorylation and ROS production

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