Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Proc Natl Acad Sci U S A
2000 Aug 29;9718:9931-6. doi: 10.1073/pnas.170153097.
Show Gene links
Show Anatomy links
Hexose permeation pathways in Plasmodium falciparum-infected erythrocytes.
Woodrow CJ
,
Burchmore RJ
,
Krishna S
.
???displayArticle.abstract???
Plasmodium falciparum requires glucose as its energy source to multiply within erythrocytes but is separated from plasma by multiple membrane systems. The mechanism of delivery of substrates such as glucose to intraerythrocytic parasites is unclear. We have developed a system for robust functional expression in Xenopus oocytes of the P. falciparum asexual stage hexose permease, PfHT1, and have analyzed substrate specificities of PfHT1. We show that PfHT1 (a high-affinity glucose transporter, K(m) approximately 1.0 mM) also transports fructose (K(m) approximately 11.5 mM). Fructose can replace glucose as an energy source for intraerythrocytic parasites. PfHT1 binds fructose in a furanose conformation and glucose in a pyranose form. Fructose transport by PfHT1 is ablated by mutation of a single glutamine residue, Q169, which is predicted to lie within helix 5 of the hexose permeation pathway. Glucose transport in the Q169N mutant is preserved. Comparison in oocytes of transport properties of PfHT1 and human facilitative glucose transporter (GLUT)1, an archetypal mammalian hexose transporter, combined with studies on cultured P. falciparum, has clarified hexose permeation pathways in infected erythrocytes. Glucose and fructose enter erythrocytes through separate permeation pathways. Our studies suggest that both substrates enter parasites via PfHT1.
Caspari,
Structure/function relationship of the Chlorella glucose/H+ symporter.
1994, Pubmed
Caspari,
Structure/function relationship of the Chlorella glucose/H+ symporter.
1994,
Pubmed
Concha,
Human erythrocytes express GLUT5 and transport fructose.
1997,
Pubmed
Desai,
Pore size of the malaria parasite's nutrient channel.
1997,
Pubmed
Fry,
Transport of D-fructose and its analogues by Trypanosoma brucei.
1993,
Pubmed
Garcia,
Amino acid substitutions at tryptophan 388 and tryptophan 412 of the HepG2 (Glut1) glucose transporter inhibit transport activity and targeting to the plasma membrane in Xenopus oocytes.
1992,
Pubmed
,
Xenbase
Geary,
Nutritional requirements of Plasmodium falciparum in culture. III. Further observations on essential nutrients and antimetabolites.
1985,
Pubmed
Gould,
Expression of a functional glucose transporter in Xenopus oocytes.
1989,
Pubmed
,
Xenbase
Gould,
The glucose transporter family: structure, function and tissue-specific expression.
1993,
Pubmed
Hashiramoto,
Site-directed mutagenesis of GLUT1 in helix 7 residue 282 results in perturbation of exofacial ligand binding.
1992,
Pubmed
Hresko,
Topology of the Glut 1 glucose transporter deduced from glycosylation scanning mutagenesis.
1994,
Pubmed
,
Xenbase
Kirk,
Transport of diverse substrates into malaria-infected erythrocytes via a pathway showing functional characteristics of a chloride channel.
1994,
Pubmed
Kirk,
Glucose uptake in Plasmodium falciparum-infected erythrocytes is an equilibrative not an active process.
1996,
Pubmed
Mueckler,
Sequence and structure of a human glucose transporter.
1985,
Pubmed
Mueckler,
Glutamine 161 of Glut1 glucose transporter is critical for transport activity and exofacial ligand binding.
1994,
Pubmed
,
Xenbase
Mueckler,
Identification of an amino acid residue that lies between the exofacial vestibule and exofacial substrate-binding site of the Glut1 sugar permeation pathway.
1997,
Pubmed
,
Xenbase
Mueckler,
Transmembrane segment 5 of the Glut1 glucose transporter is an amphipathic helix that forms part of the sugar permeation pathway.
1999,
Pubmed
,
Xenbase
Newton,
Severe falciparum malaria in children: current understanding of pathophysiology and supportive treatment.
1998,
Pubmed
Penny,
Expression of substrate-specific transporters encoded by Plasmodium falciparum in Xenopus laevis oocytes.
1998,
Pubmed
,
Xenbase
Rumsey,
Glucose transporter isoforms GLUT1 and GLUT3 transport dehydroascorbic acid.
1997,
Pubmed
,
Xenbase
Saliba,
pH regulation in the intracellular malaria parasite, Plasmodium falciparum. H(+) extrusion via a V-type H(+)-ATPase.
1999,
Pubmed
Seatter,
QLS motif in transmembrane helix VII of the glucose transporter family interacts with the C-1 position of D-glucose and is involved in substrate selection at the exofacial binding site.
1998,
Pubmed
,
Xenbase
ter Kuile,
Plasmodium falciparum: in vitro studies of the pharmacodynamic properties of drugs used for the treatment of severe malaria.
1993,
Pubmed
Woodrow,
Intraerythrocytic Plasmodium falciparum expresses a high affinity facilitative hexose transporter.
1999,
Pubmed
,
Xenbase
Wu,
Different functional domains of GLUT2 glucose transporter are required for glucose affinity and substrate specificity.
1998,
Pubmed
,
Xenbase
