Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Turning up the heat: heat stress induces markers of programmed cell death in Plasmodium falciparum in vitro

19 Dec 2013

Abstract excerpt

Malaria is characterised by cyclical febrile episodes that result from the rupture of mature schizont-infected erythrocytes releasing merozoites. In patients infected with Plasmodium falciparum, fever may reach peak temperatures as high as 41 °C. Febrile episodes typically have a deleterious effect on parasites and probably benefit the host by aiding parasite clearance; however, the parasite may also gain...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Malaria Research and Control
Share to Mosquito-borne diseases and control
Share to Vibrio bacteria research studies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 24357802
DOI: 10.1038/cddis.2013.505

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Turning up the heat: heat stress induces markers of programmed cell death in Plasmodium falciparum in vitroPMID 24357802Read ↗

Molecular Factors and Biochemical Pathways Induced by Febrile Temperature in Intraerythrocytic <i>Plasmodium falciparum</i> ParasitesSemantic proximity Read ↗

Manipulating Eryptosis of Human Red Blood Cells: A Novel Antimalarial Strategy?Semantic proximity Read ↗

Chloroquine induces eryptosis in <i>P. falciparum-infected</i> red blood cells and the release of extracellular vesicles with a unique protein profileSemantic proximity Read ↗

2-Cys peroxiredoxin of Plasmodium falciparum is involved in resistance to heat stress of the parasite.Semantic proximity Read ↗

Essential role for HSP40 in asexual replication and thermotolerance of malaria parasitesSemantic proximity Read ↗

Cell death pathways in pathogenic trypanosomatids: lessons of (over)killSemantic proximity Read ↗

Thermal and non-thermal stress conditions activate the <i>Plasmodium falciparum</i> AP2-HS-dependent heat-shock responseSemantic proximity Read ↗

A high parasite density environment induces transcriptional changes and cell death in Plasmodium falciparum blood stages.Semantic proximity Read ↗

An equivalence of prokaryotic pore forming proteins of Plasmodium triggers cellular dysfunction responsible for malaria pathogenesisSemantic proximity Read ↗

Malarial infection develops mitochondrial pathology and mitochondrial oxidative stress to promote hepatocyte apoptosisSemantic proximity Read ↗

The heat shock protein 40 family of the malaria parasite <i>Plasmodium falciparum</i>Semantic proximity Read ↗

Apoptotic markers in protozoan parasitesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.