Recently, a hydroxymethylcytosine-like modification was identified at a higher extent compared with me 5C and was linked to P. falciparum, after decades of debate the existence of methylated cytosines (me 5C) were finally identified in genomic DNA by the use of unbiased bisulfite conversion coupled with deep sequencing. In addition, 3-methyladenine and 1, N 6-ethenoadenine are able to inhibit progression of DNA replication fork and thereby the DNA replication process. MAG knockdown in animal models and cell cultures results in a modulation of sensitivity to alkylating agents. It is also known as N-methylpurine DNA glycosylase (MPG) due to its versatility in accommodating a variety of substrates in the active site. MAG orthologues are present in Escherichia coli, Saccharomyces cerevisiae, rodents, humans, and plants. The enzyme is capable of removing 3-methyladenine (m 3A) as well as other cyclic adducts in DNA, such as 1, N 6ethenoadenine (εA), 3, N 4-ethenocytosine (εC), N 2,3-ethenoguaine ( N 2,3-εG), and l, N 2-ethenoguanine (1, N 2-εG). DNA-3-methyladenine DNA glycosylase (MAG), a single sub-unit monofunctional DNA repair enzyme, belongs to an alkyladenine DNA glycosylase (AAG) superfamily, characterized by an antiparallel β-sheet and flanked by α-helices. The high A–T content of the malaria parasite genome implies the potential of these regions being modified (alkylated), thereby the need of a parasite repair enzyme. The parasite genome lacks genes encoding DNA repair enzymes in the non-homologous end joining pathway, but previous identification of PfPolδ suggests parasite base excision repair mechanism might rely mainly on a long patch repair pathway. falciparum ATP-dependent DNA helicase RuvB3 ( PfRuvB3). falciparum DNA polymerase delta ( PfPolδ) and P. falciparum uracil DNA glycosylase ( PfUGD), P. falciparum DNA repair pathway present potential drugable targets, including P. Although a malaria vaccine has recently become available, it only provides partial protection, and chemotherapeutic agents still play an essential role in malaria treatment and prevention.Īmong the various parasite targets being studied for drug development, enzymes in P. Plasmodium falciparum causes most severity in terms of clinical pathology and complication in treatment as it readily develops resistance to all existing anti-malarial agents, including most recently the artemisinins, highlighting the urgent need for identification of new parasite targets and development of safe and effective novel drugs targeting them. The World Health Organization (WHO) reported 228 million new cases of malaria in 2018, with 97% of the infection in sub-Saharan Africa caused by Plasmodium falciparum and resulting in 405,000 deaths, mainly of children. Malaria is one of the major infectious diseases threatening two-thirds of the world’s population, especially those living in tropical and sub-tropical regions, imposing both a disease and economic burden in these countries. The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made.
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