{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["El Bissati K"],"funding":["NCRR NIH HHS","NIAID NIH HHS"],"pagination":["130-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2612043"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["161(2)"],"pubmed_abstract":["The malaria parasite, Plasmodium falciparum, is unable to synthesize the purine ring de novo and is therefore wholly dependent upon purine salvage from the host for survival. Previous studies have indicated that a P. falciparum strain in which the purine transporter PfNT1 had been disrupted was unable to grow on physiological concentrations of adenosine, inosine and hypoxanthine. We have now used an episomally complemented pfnt1Delta knockout parasite strain to confirm genetically the functional role of PfNT1 in P. falciparum purine uptake and utilization. Episomal complementation by PfNT1 restored the ability of pfnt1Delta parasites to transport and utilize adenosine, inosine and hypoxanthine as purine sources. The ability of wild-type and pfnt1Delta knockout parasites to transport and ut"],"journal":["Molecular and biochemical parasitology"],"pubmed_title":["Genetic evidence for the essential role of PfNT1 in the transport and utilization of xanthine, guanine, guanosine and adenine by Plasmodium falciparum."],"pmcid":["PMC2612043"],"funding_grant_id":["M01 RR 06192","M01 RR006192-145641","M01 RR006192","R01 AI051507","M01 RR006192-137378","AI 51507"],"pubmed_authors":["El Bissati K","Horowitz M","Ullman B","Ben Mamoun C","Kim SK","Carter N","Downie MJ"],"additional_accession":[]},"is_claimable":false,"name":"Genetic evidence for the essential role of PfNT1 in the transport and utilization of xanthine, guanine, guanosine and adenine by Plasmodium falciparum.","description":"The malaria parasite, Plasmodium falciparum, is unable to synthesize the purine ring de novo and is therefore wholly dependent upon purine salvage from the host for survival. Previous studies have indicated that a P. falciparum strain in which the purine transporter PfNT1 had been disrupted was unable to grow on physiological concentrations of adenosine, inosine and hypoxanthine. We have now used an episomally complemented pfnt1Delta knockout parasite strain to confirm genetically the functional role of PfNT1 in P. falciparum purine uptake and utilization. Episomal complementation by PfNT1 restored the ability of pfnt1Delta parasites to transport and utilize adenosine, inosine and hypoxanthine as purine sources. The ability of wild-type and pfnt1Delta knockout parasites to transport and ut","dates":{"release":"2008-01-01T00:00:00Z","publication":"2008 Oct","modification":"2025-04-04T19:12:55.399Z","creation":"2019-03-27T00:19:57Z"},"accession":"S-EPMC2612043","cross_references":{"pubmed":["18639591"],"doi":["10.1016/j.molbiopara.2008.06.012"]}}