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In summary, it can be postulated that during Fe deficiency the accumulation of GSH in cells can activate the vacuolar Fe exporters like AtNRAMP3 and AtNRAMP4 to facilitate Fe export from the vacuolar reserve

Eventually, genetic deletion of TRPV2, TRPC3, Piezo1 and TRPV4 abrogated the NET formation upon PMA treatment in neutrophil-like HL-60 cells, without affecting PS externalization (Extended Data Fig