| Literature DB >> 26709459 |
Gregory LaMonte1, Katelyn A Walzer1, Joshua Lacsina2, Christopher Nicchitta2, Jen-Tsan Chi3.
Abstract
The genetic variation responsible for the sickle cell allele (HbS) enables erythrocytes to resist infection by the malaria parasite, P. falciparum. The molecular basis of this resistance, which is known to be multifactorial, remains incompletely understood. Recent studies found that the differential expression of erythrocyte microRNAs, once translocated into malaria parasites, affect both gene regulation and parasite growth. These miRNAs were later shown to inhibit mRNA translation by forming a chimeric RNA transcript via 5' RNA fusion with discreet subsets of parasite mRNAs. Here, the techniques that were used to study the functional role and putative mechanism underlying erythrocyte microRNAs on the gene regulation and translational potential of P. falciparum, including the transfection of modified synthetic microRNAs into host erythrocytes, will be detailed. Finally, a polysome gradient method is used to determine the extent of translation of these transcripts. Together, these techniques allowed us to demonstrate that the dysregulated levels of erythrocyte microRNAs contribute to cell-intrinsic malaria resistance of sickle erythrocytes.Entities:
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Year: 2015 PMID: 26709459 PMCID: PMC4692797 DOI: 10.3791/53214
Source DB: PubMed Journal: J Vis Exp ISSN: 1940-087X Impact factor: 1.355