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Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 754054, 2 pages
Comment on “Emerging Functions of Transcription Factors in Malaria Parasite"
Department of Molecular Biology and Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544-1014, USA
Received 19 January 2012; Accepted 18 March 2012
Copyright © 2012 Heather J. Painter and Manuel Llinás. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
In a recent Journal of Biomedicine and Biotechnology special issue on Immunology and Cell Biology of Parasitic Disease (2011), Tuteja et al.  authored a review summarizing transcription factors in the malaria parasite, Plasmodium. It is well known that there are very few characterized transcriptional regulators in the malaria parasite [2–4]. To date, the sole family of transcriptional regulators in Plasmodium consists of a conserved group of proteins containing a DNA-interaction domain with high homology to the Arabidopsis APETELA2 (AP2) DNA-binding domain . Related AP2-integrase DNA-binding domains are also present in various Tetrahymena species, a few viruses, and cyanobacteria (reviewed in ). However, there have been no reports of an AP2 expansion in any other eukaryote other than the Apicomplexans. This lineage-specific expansion is now known as the Apicomplexan AP2 (ApiAP2) protein family , and since these proteins represent the first family of putative specific transcriptional regulators in the malaria parasite, their characterization has generated a flurry of recent reports [7–10]. The authors of this review, unfortunately, report an incorrect association between the ApiAP2 proteins (pfam PF00847) and the Activator Protein-2 (AP-2) (pfam PF03299) found in higher eukaryotes (reviewed in ). Despite the similarity in nomenclature, there is absolutely no evolutionary conservation (homology) or functional relationship between the mammalian AP-2 and the malarial ApiAP2 proteins as the authors suggest. The authors also incorrectly cite a recent in-depth review of the ApiAP2 protein family as a source for this information . As an international journal with a diverse readership, it is pertinent that this misleading information is corrected so as to prevent further confusion.
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