Adenosine monophosphate deaminase 3 activation shortens erythrocyte half-life and provides malaria resistance in mice

Author:

Hortle Elinor1,Nijagal Brunda2,Bauer Denis C.3ORCID,Jensen Lora M.1,Ahn Seong Beom4,Cockburn Ian A.1,Lampkin Shelley1,Tull Dedreia2,McConville Malcolm J.5,McMorran Brendan J.1,Foote Simon J.1ORCID,Burgio Gaetan1ORCID

Affiliation:

1. Department of Immunology and Infectious Disease, John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia;

2. Metabolomics Australia, Bio21 Institute, University of Melbourne, Parkville, VIC, Australia;

3. Commonwealth Scientific and Industrial Research Organization, Sydney, NSW, Australia;

4. Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia; and

5. Department of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, VIC, Australia

Abstract

Key Points AMPD3 activation reduces red blood cell half-life, which is associated with increased oxidative stress and phosphatidylserine exposure. AMPD3 activation causes malaria resistance through increased RBC turnover and increased RBC production.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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