Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

55 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Parasite in vivo blood transcriptomes from Malawian children with cerebral malaria

ABSTRACT: Paper: Transcriptional Profiling of Plasmodium falciparum Parasites from Patients with Severe Malaria Identifies Distinct Low vs. High Parasitemic Clusters Milner et al Plos One July 18, 2012 Plasmodium falciparum Parasites from Patients with Severe Malaria

ORGANISM(S): Plasmodium falciparum

SUBMITTER: Johanna Daily

PROVIDER: E-GEOD-83667 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Parasite in vivo blood transcriptomes from Malawian children with cerebral malaria

Project description:Paper: Transcriptional Profiling of Plasmodium falciparum Parasites from Patients with Severe Malaria Identifies Distinct Low vs. High Parasitemic Clusters Milner et al Plos One July 18, 2012

2016-06-24 | GSE83667 | GEO

Paired whole blood human transcription profiles from children with severe malaria and mild malaria

Project description:Whole blood transcriptomes from a longitudinal study of 5 Malawian children who first present with severe Plasmodium falciparum malaria, and return in one month with mild malaria We used microarrays to identify transcripts that were associated with each clinical presentation. A blood sample was taken upon presentation during the severe and mild malaria episodes in 5 Malawian children (total n=5 pairs) followed by RNA extraction and hybridization on Affymetrix GeneChip Human Gene 1.0 ST Array, using a paired analysis

2012-01-11 | E-GEOD-33811 | biostudies-arrayexpress

Paired whole blood human transcription profiles from children with severe malaria and mild malaria

2012-01-11 | GSE33811 | GEO

Discovery of telomere repeat-binding factor in the malaria parasite Plasmodium falciparum

Project description:ChIP-seq experiments were performed for the putative telomere repeat-binding factor (PfTRF) in the malaria parasite Plasmodium falciparum strain 3D7. The gene encoding this factor (PF3D7_1209300) was endogenously tagged with either a GFP- or a 3xHA-tag and these transgenic parasite lines were used in ChIP-sequencing experiments. Sequencing of the ChIP and input libraries showed enrichment of PfTRF at all telomere-repeat containing chromosome ends (reference genome Plasmodium falciparum 3D7 from PlasmoDB version 6.1) as well as in all upsB var promoters.In addition,PfTRF was enriched at seven additional, intra-chromosomal sites and called in the PfTRF-HA ChIP-seq only. Plasmodium falciparum 3D7 parasites were generated with -GFP or -3xHA C-terminal tagged TRF (PF3D7_1209300). Nuclei were isolated from formaldehyde cross-linked schizont-stage transgenic parasites and used to prepare chromatin. Chromatin immunoprecipitations were performed using mouse anti-GFP (Roche Diagnostics, #11814460001) or rat anti-HA 3F10 (Roche Diagnostics, #12158167001). Sequencing libraries were prepared according to a Plasmodium-optimized library preparation procedure including KAPA polymerase-mediated PCR amplification.

2016-07-15 | E-GEOD-76537 | biostudies-arrayexpress

Bulk RNA-seq of the human malaria parasite Plasmodium falciparum 3D7 cultured under different iron conditions

Project description:Background: Host iron deficiency is protective against severe malaria as the human malaria parasite Plasmodium falciparum depends on free iron from its host to proliferate. Due to the absence of transferrin, ferritin, ferroportin, and a functional heme oxygenase, the parasite’s essential pathways of iron acquisition, storage, export, and detoxification differ from those in humans and may thus be excellent targets for therapeutic development. However, the proteins involved in these processes in P. falciparum remain largely unknown. Experimental design: To identify iron-regulated mechanisms and putative iron transporters in the human malaria parasite Plasmodium falciparum 3D7, we carried out whole-transcriptome profiling using bulk RNA-sequencing. The parasites were cultured either using erythrocytes from a donors with high, medium (healthy) or low iron status (experiment 1); or with red blood cells from another healthy donor in the presence or absence of 0.7 µM hepcidin, a specific ferroportin inhibitor and iron-regulatory hormone (experiment 2). This concentration of hepcidin was reported to reduce binding of ferrous iron to ferroportin by 50% in vitro (39). Samples from three biological replicates each were harvested at the ring and trophozoite stage (6 – 9 and 26 – 29 hours post invasion, hpi) during the second intra-erythrocytic developmental cycle under the conditions specified.

2024-04-08 | E-MTAB-13411 | biostudies-arrayexpress

Replication origin mapping in the malaria parasite P. falciparum

Project description:Replication origin mapping in the malaria parasite Plasmodium falciparum

2022-08-04 | GSE210010 | GEO

Population structure shapes copy number variation in malaria parasites

Project description:If copy number variants (CNVs) are predominantly deleterious, we would expect them to be more efficiently purged from populations with a large effective population size (Ne) than from populations with a small Ne. Malaria parasites (Plasmodium falciparum) provide an excellent organism to examine this prediction, because this protozoan shows a broad spectrum of population structures within a single species, with large, stable, outbred populations in Africa, small unstable inbred populations in South America and with intermediate population characteristics in South East Asia. We characterized 122 single-clone parasites, without prior laboratory culture, from malaria-infected patients in 7 countries in Africa, SE Asia and S. America using a high density SNP/CNV microarray. We scored 134 high-confidence CNVs across the parasite exome, including 33 deletions and 102 amplifications, which ranged in size from <500bp to 59kb, as well as 10,107 flanking, biallelic SNPs. Overall, CNVs were rare, small and skewed towards low frequency variants, consistent with the deleterious model. Relative to African and SE Asian populations, CNVs were significantly more common in S. America, showed significantly less skew in allele frequencies, and were significantly larger. On this background of low frequency CNV, we also identified several high-frequency CNVs under putative positive selection using an FST outlier analysis. These included known adaptive CNVs containing rh2b and pfmdr1, and several other CNVs (e.g. DNA helicase, and 3 conserved proteins) that require further investigation. Our data are consistent with a significant impact of genetic structure on CNV burden in an important human pathogen. SNP/CGH hybridisation of 175 malaria parasite samples

2015-11-19 | E-GEOD-75137 | biostudies-arrayexpress

Targeting Circulating Labile Heme as a Defense Strategy Against Malaria

Project description:Severe presentations of malaria emerge as parasites from Plasmodium spp. proliferate and lyse red blood cells (RBC), producing extracellular hemoglobin (HB). The heme prosthetic groups are released upon HB oxidation generating circulating labile heme. Here we asked whether scavenging of extracellular HB and/or labile heme, by haptoglobin (HP) and/or hemopexin (HPX), respectively, is protective against severe presentations of malaria. We found that circulating labile heme is an independent risk factor for cerebral and non-cerebral severe presentations of P. falciparum malaria. Labile heme was negatively correlated with HP and HPX, which were however, not risk factors for severe P. falciparum malaria. Genetic HP and/or HPX deletion in mice led to accumulation of labile heme in plasma and kidneys in response to Plasmodium (chabaudi chabaudi) infection. This was associated with increased mortality and acute kidney injury (AKI) in ageing but not adult mice, corroborated in P. falciparum malaria by a an inverse correlation between HPX and heme with serological markers of AKI. In conclusion, HP and HPX exert an age-dependent protective effect against malaria that counters the pathogenesis of AKI in mice and presumably in humans.

2024-01-30 | GSE253390 | GEO

Expression data from whole blood samples of Rwandan adults with mild malaria with matched sample thirty days later (convalescence)

Project description:Host factors governing mild disease in adults who have developed clinical immunity to Plasmodium falciparum may provide insights for disease altering vaccine or interventions, to prevent severe malaria We used microarrays of whole blood samples during mild malaria and compared them in a paired analysis to whole blood microarray 30 days later. (n=19 pairs) 3mL of whole blood was immediately placed in Tri-Reagent BD, frozen; high quality pairs were selected, were randomly selected for hybridization and analysis. Sense strand cDNA was generated from total RNA using the Ambion® WT Expression Kit (Life Technologies, Grand Island, NY) and labeling was done with the GeneChip® WT Terminal Labeling Kit (Affymetrix, Santa Clara, CA) for use with the GeneChip® Human Gene 1.0 ST Arrays (Affymetrix). The array image was generated by a high-resolution GeneArray Scanner 3000 7G (Affymetrix).

2014-12-19 | E-GEOD-64338 | biostudies-arrayexpress

Global gene expression of the rodent malaria parasites Plasmodium yoelii, Plasmodium berghei and Plasmodium chabaudi blood-stage parasites

Project description:The purpose of this research is to identify and evaluate the global gene expression of the rodent malaria parasites Plasmodium yoelii, Plasmodium berghei and Plasmodium chabaudi blood-stage parasites and specifically compare the blood stage gene expression profiles of samples derived from previous studies on Plasmodium falciparum, Plasmodium vivax and Plasmodium knowlesi

2016-04-08 | GSE80015 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data