@article {538831,
	title = {Epigenetic memory at malaria virulence genes},
	journal = {Proc Natl Acad Sci U S A},
	volume = {104},
	number = {3},
	year = {2007},
	note = {<p>Chookajorn, ThanatDzikowski, RonFrank, MatthiasLi, FelomenaJiwani, Alisha ZHartl, Daniel LDeitsch, Kirk WengAI 52390/AI/NIAID NIH HHS/Research Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov{\textquoteright}t2007/01/09 09:00Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):899-902. Epub 2007 Jan 5.</p>},
	month = {Jan 16},
	pages = {899-902},
	abstract = {<p>During its red blood cell stage, the malaria parasite Plasmodium falciparum can switch its variant surface proteins (P. falciparum erythrocyte membrane protein 1) to evade the host immune response. The var gene family encodes P. falciparum erythrocyte membrane protein 1, different versions of which have unique binding specificities to various human endothelial surface molecules. Individual parasites each contain approximately 60 var genes at various locations within their chromosomes; however, parasite isolates contain different complements of var genes, thus, the gene family is enormous with a virtually unlimited number of members. A single var gene is expressed by each parasite in a mutually exclusive manner. We report that control of var gene transcription and antigenic variation is associated with a chromatin memory that includes methylation of histone H3 at lysine K9 as an epigenetic mark. We also discuss how gene transcription memory may affect the mechanism of pathogenesis and immune evasion.</p>},
	keywords = {*Gene Expression Regulation, Animals, Chromatin/genetics/metabolism, Epigenesis, Genetic/*genetics, Histones/metabolism, Malaria/immunology/*parasitology, Methylation, Plasmodium falciparum/*genetics/immunology/*pathogenicity, Transcription, Genetic/genetics, Virulence/genetics},
	isbn = {0027-8424 (Print)0027-8424 (Linking)},
	author = {Chookajorn, T. and Dzikowski, R. and Frank, M. and Li, F. and Jiwani, A. Z. and Hartl, D. L. and Deitsch, K. W.}
}
