16alpha-bromoepiandrosterone, a dehydroepiandrosterone (DHEA) analogue, inhibits Plasmodium falciparum and Plasmodium berghei growth.

2000 ◽  
Vol 63 (5) ◽  
pp. 280-283 ◽  
Author(s):  
D Freilich ◽  
D Nelson ◽  
S Ferris ◽  
C Ahlem ◽  
J Hebert ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Plasmodium Berghei

The putative gene for the first enzyme of glutathione biosynthesis in Plasmodium berghei and Plasmodium falciparum

1999 ◽  
Vol 99 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Cecilia Birago ◽  
Tomasino Pace ◽  
Leonardo Picci ◽  
Elisabetta Pizzi ◽  
Raffaella Scotti ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Plasmodium Berghei ◽  
Putative Gene ◽  
Glutathione Biosynthesis

Antimalarial Activity of Phenazines from Lapachol, β-Lapachone and Its Derivatives Against Plasmodium falciparum in vitro and Plasmodium berghei in vivo.

ChemInform ◽  
2004 ◽  
Vol 35 (26) ◽  
Author(s):  
Valter F. de Andrade-Neto ◽  
Marilia O. F. Goulart ◽  
Jorge F. da Silva Filho ◽  
Matuzalem J. da Silva ◽  
Maria do Carmo F. R. Pinto ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Plasmodium Berghei ◽  
Antimalarial Activity

Aminopeptidases from Plasmodium falciparum, Plasmodium chabaudi chabaudi and Plasmodium berghei

1994 ◽  
Vol 41 (2) ◽  
pp. 119-123 ◽  
Author(s):  
G. PAUL CURLEY ◽  
SUSAN M. O'DONOVAN ◽  
JOHN MCNALLY ◽  
MARGARET MULLALLY ◽  
HELEN O'HARA ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Plasmodium Berghei ◽  
Plasmodium Chabaudi

Solution Combustion Synthesis of Hierarchically Structured V2O5 Nanoflakes: Efficacy Against Plasmodium falciparum, Plasmodium berghei and the Malaria Vector Anopheles stephensi

2017 ◽  
Vol 28 (4) ◽  
pp. 2337-2348 ◽  
Author(s):  
Kadarkarai Murugan ◽  
Christina Mary Samidoss ◽  
Jayaraman Theerthagiri ◽  
Chellasamy Panneerselvam ◽  
Jagannathan Madhavan ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Combustion Synthesis ◽  
Malaria Vector ◽  
Plasmodium Berghei ◽  
Anopheles Stephensi ◽  
Solution Combustion Synthesis ◽  
Solution Combustion

scholarly journals Genetic alteration of ferredoxin NADP+-reductase or cysteine desulfurase in piperaquine-resistant Plasmodium berghei restores susceptibility to lumefantrine and abolishes the impact of probenecid, verapamil, and cyproheptadine

2019 ◽  
Author(s):  
Fagdéba David Bara ◽  
Loise Ndung’u ◽  
Noah Machuki Onchieku ◽  
Beatrice Irungu ◽  
Simplice Damintoti Karou ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Plasmodium Berghei ◽  
Malaria Parasite ◽  
Drug Action ◽  
Cysteine Desulfurase ◽  
Human Malaria Parasite ◽  
Human Malaria ◽  
Essential Components ◽  
The Impact

AbstractChemotherapy remains central in the control of malaria; however, resistance has consistently thwarted these efforts. Currently, lumefantrine (LM), and piperaquine (PQ) drugs, are essential components in the mainstay artemisinin-based therapies used for the treatment of malaria globally. Using LM and PQ-resistant Plasmodium berghei, we measured the effect of known chemosensitizers: probenecid, verapamil, or cyproheptadine on the activity of LM or PQ. Using PlasmoGEM vectors, we then evaluated the impact of deleting cysteine desulfurase (SufS) or over-expressing Ferredoxin NADP+ reductase (FNR), genes that mediate drug action. Our data showed that, only cyproheptadine at 5mgkg−1 restored LM activity by above 65% against the LM-resistant parasites (LMR) but failed to reinstate PQ activity against the PQ-resistant parasites (PQR). Whereas the PQR had lost significant susceptibility to LM, the three chemosensitizers; cyproheptadine, probenecid, and verapamil, restored LM potency against the PQR by above 70%, 60%, and 55% respectively. We thus focused on LM resistance in PQR. Deletion of the SufS or overexpression of the FNR genes in the PQR abolished the impact of the chemosensitizers on the LM activity, and restored the susceptibility of the PQR parasites to LM. Taken together, we demonstrate the association between SufS or FNR genes with the action of LM and chemosensitizers in PQR parasites. There is, however, need to interrogate the impact of the chemosensitizers and the role of SufS or FNR genes on LM action in the human malaria parasite, Plasmodium falciparum.

scholarly journals Identification of Three Novel Plasmodium Factors Involved in Ookinete to Oocyst Developmental Transition

2021 ◽  
Vol 11 ◽  
Author(s):  
Chiamaka V. Ukegbu ◽  
George K. Christophides ◽  
Dina Vlachou
Keyword(s):  
Plasmodium Falciparum ◽  
Plasmodium Berghei ◽  
Disease Transmission ◽  
Sub Saharan Africa ◽  
Parasite Transmission ◽  
Targeted Disruption ◽  
Transmission Blocking ◽  
Essential Function ◽  
Sub Saharan ◽  
Transmission Biology

Plasmodium falciparum malaria remains a major cause of global morbidity and mortality, mainly in sub-Saharan Africa. The numbers of new malaria cases and deaths have been stable in the last years despite intense efforts for disease elimination, highlighting the need for new approaches to stop disease transmission. Further understanding of the parasite transmission biology could provide a framework for the development of such approaches. We phenotypically and functionally characterized three novel genes, PIMMS01, PIMMS57, and PIMMS22, using targeted disruption of their orthologs in the rodent parasite Plasmodium berghei. PIMMS01 and PIMMS57 are specifically and highly expressed in ookinetes, while PIMMS22 transcription starts already in gametocytes and peaks in sporozoites. All three genes show strong phenotypes associated with the ookinete to oocyst transition, as their disruption leads to very low numbers of oocysts and complete abolishment of transmission. PIMMS22 has a secondary essential function in the oocyst. Our results enrich the molecular understanding of the parasite-vector interactions and identify PIMMS01, PIMMS57, and PIMMS22 as new targets of transmission blocking interventions.

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