Evidence map›Paper›PMID 17517609›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Effect of plasmodial RESA protein on deformability of human red blood cells harboring Plasmodium falciparum.

J P Mills, M Diez-Silva, D J Quinn, M Dao, M J Lang, K S W Tan, C T Lim, G Milon, P H David, O Mercereau-Puijalon and 2 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

87 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Biomechanics of phagocytosis of red blood cells by macrophages in the human spleen.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Cells · 2024
    Review
  6. Identification of ExportedMicroorganisms · 2022
    Article
  7. Exported J domain proteins of the human malaria parasite.Frontiers in molecular biosciences · 2022
    Review
  8. Biophysical Tools and Concepts Enable Understanding of Asexual Blood Stage Malaria.Frontiers in cellular and infection microbiology · 2022
    Review
  9. Article
  10. Article
  11. Heat Shock Proteins as Targets for Novel Antimalarial Drug Discovery.Advances in experimental medicine and biology · 2021
    Article
  12. Host Cytoskeleton Remodeling throughout the Blood Stages of Plasmodium falciparum.Microbiology and molecular biology reviews : MMBR · 2019
    Review
  13. Review
  14. Mechanical fatigue of human red blood cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Article
  16. Review
  17. Erythrocyte Membrane Makeover byFrontiers in microbiology · 2019
    Review
  18. Review
  19. Hemoglobin E, malaria and natural selection.Evolution, medicine, and public health · 2019
    Review
  20. Article

27 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

J P MillsDepartment of Materials Science and Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
M Diez-Silva
D J Quinn
M Dao
M J Lang
K S W Tan
C T Lim
G Milon
P H David
O Mercereau-Puijalon
S Bonnefoy
S Suresh

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During intraerythrocytic development, Plasmodium falciparum exports proteins that interact with the host cell plasma membrane and subplasma membrane-associated spectrin network. Parasite-exported proteins modify mechanical properties of host RBCs, resulting in altered cell circulation. In this work, optical tweezers experiments of cell mechanical properties at normal physiological and febrile temperatures are coupled, for the first time, with targeted gene disruption techniques to measure the effect of a single parasite-exported protein on host RBC deformability. We investigate Pf155/Ring-infected erythrocyte surface antigen (RESA), a parasite protein transported to the host spectrin network, on deformability of ring-stage parasite-harboring human RBCs. Using a set of parental, gene-disrupted, and revertant isogenic clones, we found that RESA plays a major role in reducing deformability of host cells at the early ring stage of parasite development, but not at more advanced stage. We also show that the effect of RESA on deformability is more pronounced at febrile temperature, which ring-stage parasite-harboring RBCs can be exposed to during a malaria attack, than at normal body temperature.

Indexed as

Cell ShapeAnimalsErythrocytesHumansPlasmodium falciparumProtozoan ProteinsTemperatureTrophozoitesProtozoan Proteinsring-infected erythrocyte surface antigen (RESA), Plasmodium falciparum

Identifiers

PMID17517609
PMCPMC1874230

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.