↓ Skip to main content

Suppression of experimental cerebral malaria by disruption of malate:quinone oxidoreductase

Overview of attention for article published in Malaria Journal, June 2017
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age

Mentioned by

twitter
3 tweeters

Citations

dimensions_citation
14 Dimensions

Readers on

mendeley
31 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Suppression of experimental cerebral malaria by disruption of malate:quinone oxidoreductase
Published in
Malaria Journal, June 2017
DOI 10.1186/s12936-017-1898-5
Pubmed ID
Authors

Mamoru Niikura, Keisuke Komatsuya, Shin-Ichi Inoue, Risa Matsuda, Hiroko Asahi, Daniel Ken Inaoka, Kiyoshi Kita, Fumie Kobayashi

Abstract

Aspartate, which is converted from oxaloacetate (OAA) by aspartate aminotransferase, is considered an important precursor for purine salvage and pyrimidine de novo biosynthesis, and is thus indispensable for the growth of Plasmodium parasites at the asexual blood stages. OAA can be produced in malaria parasites via two routes: (i) from phosphoenolpyruvate (PEP) by phosphoenolpyruvate carboxylase (PEPC) in the cytosol, or (ii) from fumarate by consecutive reactions catalyzed by fumarate hydratase (FH) and malate:quinone oxidoreductase (MQO) in the mitochondria of malaria parasites. Although PEPC-deficient Plasmodium falciparum and Plasmodium berghei (rodent malaria) parasites show a growth defect, the mutant P. berghei can still cause experimental cerebral malaria (ECM) with similar dynamics to wild-type parasites. In contrast, the importance of FH and MQO for parasite viability, growth and virulence is not fully understood because no FH- and MQO-deficient P. falciparum has been established. In this study, the role of FH and MQO in the pathogenicity of asexual-blood-stage Plasmodium parasites causing cerebral malaria was examined. First, FH- and MQO-deficient parasites were generated by inserting a luciferase-expressing cassette into the fh and mqo loci in the genome of P. berghei ANKA strain. Second, the viability of FH-deficient and MQO-deficient parasites that express luciferase was determined by measuring luciferase activity, and the effect of FH or MQO deficiency on the development of ECM was examined. While the viability of FH-deficient P. berghei was comparable to that of control parasites, MQO-deficient parasites exhibited considerably reduced viability. FH activity derived from erythrocytes was also detected. This result and the absence of phenotype in FH-deficient P. berghei parasites suggest that fumarate can be metabolized to malate by host or parasite FH in P. berghei-infected erythrocytes. Furthermore, although the growth of FH- and MQO-deficient parasites was impaired, the development of ECM was suppressed only in mice infected with MQO-deficient parasites. These findings suggest that MQO-mediated mitochondrial functions are required for development of ECM of asexual-blood-stage Plasmodium parasites.

Twitter Demographics

The data shown below were collected from the profiles of 3 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 31 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 31 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 23%
Researcher 5 16%
Student > Master 4 13%
Other 2 6%
Professor 2 6%
Other 5 16%
Unknown 6 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 6 19%
Agricultural and Biological Sciences 5 16%
Pharmacology, Toxicology and Pharmaceutical Science 4 13%
Medicine and Dentistry 3 10%
Immunology and Microbiology 3 10%
Other 3 10%
Unknown 7 23%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 14 June 2017.
All research outputs
#6,505,779
of 11,364,689 outputs
Outputs from Malaria Journal
#2,168
of 3,354 outputs
Outputs of similar age
#127,935
of 267,288 outputs
Outputs of similar age from Malaria Journal
#112
of 125 outputs
Altmetric has tracked 11,364,689 research outputs across all sources so far. This one is in the 40th percentile – i.e., 40% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,354 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.2. This one is in the 31st percentile – i.e., 31% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 267,288 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 48th percentile – i.e., 48% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 125 others from the same source and published within six weeks on either side of this one. This one is in the 6th percentile – i.e., 6% of its contemporaries scored the same or lower than it.