ArticleNature microbiology2021
A heat-shock response regulated by the PfAP2-HS transcription factor protects human malaria parasites from febrile temperatures.
Article in Nature microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 56 citations in OpenAlex.
- Extracellular vesicles participate in proteostasis and heat shock adaptation inEmerging microbes & infections · 2026Article
- AP2-HS and a GDV1 regulatory feedback loop mediate environmental induction of sexual conversion in Plasmodium falciparum.Nature microbiology · 2026Article
- The DNA-binding protein PfAP2-V regulates erythrocyte invasion and pathogenesis of the human malaria parasite Plasmodium falciparum.Science China. Life sciences · 2026Article
- Characterisation of the thermal and non-thermal stress conditions that activate the Plasmodium falciparum AP2-HS-dependent heat-shock response.PLoS pathogens · 2026Article
- Physiological febrile heat stress increases cytoadhesion through increased protein trafficking ofeLife · 2026Article
- Genome-wide analysis of strand-specific transcription and DNA methylation inFrontiers in microbiology · 2026Article
- Hsp90 and associates shaping parasite biology.mSphere · 2025Review
- Circadian Biology in Parasites: Beyond Known Mechanisms.Annual review of microbiology · 2025Review
- Evolutionary Trajectory ofBiomedicines · 2025Review
- Biochemistry of Heat Shock Proteins From Human Intracellular Protozoan Parasites as Diagnostic and Therapeutic Biomarkers.Biochemistry · 2025Review
- Nucleotide-resolution Mapping of RNA N6-Methyladenosine (m6A) modifications and comprehensive analysis of global polyadenylation events in mRNA 3' end processing in malaria pathogenbioRxiv : the preprint server for biology · 2025Article
- Multiplication rate variation of malaria parasites from hospital cases and community infections.Scientific reports · 2025Article
- Overexpression inFrontiers in cellular and infection microbiology · 2025Article
- Artemisinin-resistant malaria.Clinical microbiology reviews · 2024Review
- Population genomics and transcriptomics of Plasmodium falciparum in Cambodia and Vietnam uncover key components of the artemisinin resistance genetic background.Nature communications · 2024Article
- Genome-wide analysis of the HSF family in Allium sativum L. and AsHSFB1 overexpression in Arabidopsis under heat stress.BMC genomics · 2024Article
- Unraveling the complexities of ApiAP2 regulation in Plasmodium falciparum.Trends in parasitology · 2024Review
- Infection length and host environment influence on Plasmodium falciparum dry season reservoir.EMBO molecular medicine · 2024Article
- tRNA modification reprogramming contributes to artemisinin resistance in Plasmodium falciparum.Nature microbiology · 2024Article
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8 authors at 5 institutions in 4 countries.
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Abstract
Periodic fever is a characteristic clinical feature of human malaria, but how parasites survive febrile episodes is not known. Although the genomes of Plasmodium species encode a full set of chaperones, they lack the conserved eukaryotic transcription factor HSF1, which activates the expression of chaperones following heat shock. Here, we show that PfAP2-HS, a transcription factor in the ApiAP2 family, regulates the protective heat-shock response in Plasmodium falciparum. PfAP2-HS activates the transcription of hsp70-1 and hsp90 at elevated temperatures. The main binding site of PfAP2-HS in the entire genome coincides with a tandem G-box DNA motif in the hsp70-1 promoter. Engineered parasites lacking PfAP2-HS have reduced heat-shock survival and severe growth defects at 37 °C but not at 35 °C. Parasites lacking PfAP2-HS also have increased sensitivity to imbalances in protein homeostasis (proteostasis) produced by artemisinin, the frontline antimalarial drug, or the proteasome inhibitor epoxomicin. We propose that PfAP2-HS contributes to the maintenance of proteostasis under basal conditions and upregulates specific chaperone-encoding genes at febrile temperatures to protect the parasite against protein damage.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.