z-logo
open-access-imgOpen Access
Adenosine Triphosphate Depletion of Erythrocytes Simulates the Phenotype Associated with Pyruvate Kinase Deficiency and Confers Protection againstPlasmodium falciparumIn Vitro
Author(s) -
Kodjo Ayi,
W. Conrad Liles,
Philippe Gros,
Kevin C. Kain
Publication year - 2009
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/605843
Subject(s) - pyruvate kinase , pyruvate kinase deficiency , adenosine triphosphate , plasmodium falciparum , biology , glycolysis , red blood cell , in vitro , biochemistry , phagocytosis , microbiology and biotechnology , enzyme , immunology , malaria
Erythrocytes from individuals with pyruvate kinase deficiency (PKD) are resistant to invasion by Plasmodium falciparum parasites, and erythrocytes infected with ring-stage parasites are preferentially cleared by macrophages in vitro. However, the underlying molecular basis of protection is unknown. In the present study, we examined adenosine triphosphate (ATP) levels in PKD erythrocytes (ie, erythrocytes from individuals with PKD) and determined whether depletion of ATP in normal erythrocytes would recapitulate the phenotype observed with PKD.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom