Molecular interaction of artemisinin with translationally controlled tumor protein (TCTP) of Plasmodium falciparum

Eichhorn, Tolga; Winter, Dominic; Büchele, Berthold; Dirdjaja, Natalie; Frank, Martin; Lehmann, Wolf-Dieter; Mertens, Rolf; Krauth‐Siegel, R. Luise; Simmet, Thomas; Granzin, Joachim; Efferth, Thomas

doi:10.1016/j.bcp.2012.10.006

Cited by 62 publications

(47 citation statements)

References 33 publications

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“…Genes putatively associated with ART resistance ( Pfcrt 23,24 , Pftctp 25,26 , Pfmdr1 8,27,28 , Pfmrp1 27–29 and ABC transporters 30 ) or encoding putative targets of ART ( PfATPase6 31,32 and Pfubcth —the orthologue of Plasmodium chabaudi ubp1 33,34 ) were not mutated during the 5-year selection of F32-ART5, and Pfmdr1 amplification was not observed 35–40 . In addition, all candidate ART resistance genes recently identified using population genetics approaches 14,40,41 remained unaltered in F32-ART5, except for PF3D7 _ 1343700 and PF3D7 _ 1459600 located in the linkage-disequilibrium windows identified in ref.…”

Section: Discussionmentioning

confidence: 99%

A molecular marker of artemisinin-resistant Plasmodium falciparum malaria

Ariey

Witkowski

Amaratunga

et al. 2013

Nature

1,761

2,266

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Plasmodium falciparum resistance to artemisinin derivatives in southeast Asia threatens malaria control and elimination activities worldwide. To monitor the spread of artemisinin resistance, a molecular marker is urgently needed. Here, using whole-genome sequencing of an artemisinin-resistant parasite line from Africa and clinical parasite isolates from Cambodia, we associate mutations in the PF3D7_1343700 kelch propeller domain (‘K13-propeller’) with artemisinin resistance in vitro and in vivo. Mutant K13-propeller alleles cluster in Cambodian provinces where resistance is prevalent, and the increasing frequency of a dominant mutant K13-propeller allele correlates with the recent spread of resistance in western Cambodia. Strong correlations between the presence of a mutant allele, in vitro parasite survival rates and in vivo parasite clearance rates indicate that K13-propeller mutations are important determinants of artemisinin resistance. K13-propeller polymorphism constitutes a useful molecular marker for large-scale surveillance efforts to contain artemisinin resistance in the Greater Mekong Subregion and prevent its global spread.

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Section: Discussionmentioning

confidence: 99%

A molecular marker of artemisinin-resistant Plasmodium falciparum malaria

Ariey

Witkowski

Amaratunga

et al. 2013

Nature

1,761

2,266

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“…It has been reported that artemisinins specifically and selectively inhibit Pf-ATP6, the sarco/endoplasmic reticulum Ca 2+ -ATPase [125], and Pf-PI3K, the phosphatidylinositol-3-kinase [126], of P. falciparum . Bhisutthibhan and others reported that DHA, but not its inactive congener deoxydihydroartemisinin, covalently binds Pf-fortilin TCTP in the presence of hemin, suggesting that Pf-fortilin TCTP is another molecular target of artemisinins [127, 128], as also supported by Eichhorn and coworkers [129]. To test whether DHA also binds and inhibits human fortilin TCTP , we subjected human fortilin TCTP fused to glutathione S-transferase (GST) to surface plasmon resonance binding assays.…”

Section: Fortilintctp In Human Diseases and Developmental Abnormalmentioning

confidence: 91%

Fortilin: A Potential Target for the Prevention and Treatment of Human Diseases

Pinkaew

Fujise

2017

Advances in Clinical Chemistry

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Fortilin is a highly conserved 172-amino-acid polypeptide found in the cytosol, nucleus, mitochondria, extracellular space, and circulating blood. It is a multifunctional protein that protects cells against apoptosis, promotes cell growth and cell cycle progression, binds calcium (Ca2+), and has anti-pathogen activities. Its role in the pathogenesis of human and animal diseases is also diverse. Fortilin facilitates the development of atherosclerosis, contributes to both systemic and pulmonary arterial hypertension, participates in the development of cancers, and worsens diabetic nephropathy. It is important for the adaptive expansion of pancreatic β-cells in response to obesity and increased insulin requirement, for the regeneration of liver after hepatectomy, and for protection of the liver against alcohol- and ER stress-induced injury. Fortilin is a viable surrogate marker for in vivo apoptosis, and it plays a key role in embryo and organ development in vertebrates. In fish and shrimp, fortilin participates in host defense against bacterial and viral pathogens. Further translational research could prove fortilin to be a viable molecular target for treatment of various human diseases including and not limited to atherosclerosis, hypertension, certain tumors, diabetes mellitus, diabetic nephropathy, hepatic injury, and aberrant immunity and host defense.

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“…[10][11][12][13] Regarding the diseases malaria and cancer, its mode of action is believed to be due to the endoperoxide bridge. [8,[14][15][16][17] In case of human cytomegalovirus (HCMV), a similar mechanism might be responsible for the antiviral activity considering the fact that reactive oxygen intermediates are regulators of the activity of cellular redox-sensitive factors, such as NF-κB. [18] The anti-malaria drug artesunate inhibits replication of cytomegalovirus in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 98%