Picot, S., Burnod, J., Bracchi, V., Chumpitazi, B.F. and Ambroise-Thomas, P. (1997) Apoptosis Related to Chloroquine Sensitivity of the Human Malaria Parasite Plasmodium falciparum. Transactions of the Royal Society of Tropical Medicine and Hygiene, 91, 590-591.
https://doi.org/10.1016/S0035-9203(97)90039-0

has been cited by the following article:

• TITLE: Cell-Cycle-Associated Amplified Genomic-DNA Fragments (CAGFs) Might Be Involved in Chloroquine Action and Resistance in Plasmodium falciparum

  AUTHORS: Gao-De Li

  KEYWORDS: Plasmodium falciparum, Chloroquine Resistance, Cell-Cycle-Associated Amplified Genomic-DNA Fragment (CAGF), Plasmodium falciparum Cystine Transporter (Pfct), Glutathione (GSH), Reactive Oxygen Species (ROS), Pfcrmp

  JOURNAL NAME: Open Access Library Journal, Vol.4 No.3, March 14, 2017

  ABSTRACT: As a cheap and safe antimalarial agent, chloroquine (CQ) has been used in the battle against malaria for more than half century. However, the mechanism of CQ action and resistance in Plasmodium falciparum remains elusive. Based on further analysis of our published experimental results, we propose that the mechanism of CQ action and resistance might be closely linked with cell-cycle-associated amplified genomic-DNA fragments (CAGFs, singular form = CAGF) as CQ induces CAGF production in P. falciparum, which could affect multiple biological processes of the parasite, and thus might contribute to parasite death and CQ resistance. Recently, we found that CQ induced one of CAGFs, UB1-CAGF, might downregulate a probable P. falciparum cystine transporter (Pfct) gene expression, which could be used to understand the mechanism of CQ action and resistance in P. falciparum.