Evidence map›Paper›PMID 25184562›Full record

ReviewMicrobiology and molecular biology reviews : MMBR2014

DNA repair mechanisms and their biological roles in the malaria parasite Plasmodium falciparum.

Andrew H Lee, Lorraine S Symington, David A Fidock

Abstract readReview
In one paragraph

Review in Microbiology and molecular biology reviews : MMBR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing 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

65 citing papers in PubMed.

  1. Article
  2. mSphere · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Retracing the evolution ofMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  10. Article
  11. iScience · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

5 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

3 authors.

Andrew H LeeDepartment of Microbiology and Immunology, Columbia University, New York, New York, USA.
Lorraine S SymingtonDepartment of Microbiology and Immunology, Columbia University, New York, New York, USA.
David A FidockDepartment of Microbiology and Immunology, Columbia University, New York, New York, USA Division of Infectious Diseases, Department of Medicine, Columbia University, New York, New York, USA df2260@columbia.edu.

Funding

Mechanisms of Homologous Recombination in YeastR01GM041784 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SYMINGTON, LORRAINE S · 1989 to 2017
$7.8M
Role of pfcrt in chloroquine resistance in P. falciparumR01AI050234 · NIAID · YESHIVA UNIVERSITY · PI FIDOCK, DAVID A · 2001 to 2015
$5.7M
Defining the Role of PfCRT and PfMDR1 as Pleiotropic Mediators of Plasmodium falciparum Multidrug ResistanceR37AI050234 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI David A Fidock · 2018 to 2026
$4.4M
Defining P. falciparum resistance to artemisinin-based combination therapiesR01AI109023 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FIDOCK, DAVID A · 2014 to 2025
$4.4M
Break-induced replication and genome rearrangementsR01GM094386 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SYMINGTON, LORRAINE S · 2010 to 2017
$2.4M
Columbia University Graduate Training Program in Microbiology and ImmunologyT32AI106711 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Nicholas Arpaia, Uttiya Basu · 2014 to 2026
$2.1M
NIAID NIH HHS AI109023NIAID NIH HHS R01 AI050234NIAID NIH HHS R01 AI109023NIAID NIH HHS R01AI50234NIAID NIH HHS R37 AI050234NIAID NIH HHS T32 AI106711NIGMS NIH HHS GM041784NIGMS NIH HHS GM094386NIGMS NIH HHS R01 GM041784NIGMS NIH HHS R01 GM094386
6 · The paper itself

Abstract

Research into the complex genetic underpinnings of the malaria parasite Plasmodium falciparum is entering a new era with the arrival of site-specific genome engineering. Previously restricted only to model systems but now expanded to most laboratory organisms, and even to humans for experimental gene therapy studies, this technology allows researchers to rapidly generate previously unattainable genetic modifications. This technological advance is dependent on DNA double-strand break repair (DSBR), specifically homologous recombination in the case of Plasmodium. Our understanding of DSBR in malaria parasites, however, is based largely on assumptions and knowledge taken from other model systems, which do not always hold true in Plasmodium. Here we describe the causes of double-strand breaks, the mechanisms of DSBR, and the differences between model systems and P. falciparum. These mechanisms drive basic parasite functions, such as meiosis, antigen diversification, and copy number variation, and allow the parasite to continually evolve in the contexts of host immune pressure and drug selection. Finally, we discuss the new technologies that leverage DSBR mechanisms to accelerate genetic investigations into this global infectious pathogen.

Indexed as

DNA RepairAnimalsAntimalarialsDNA Breaks, Double-StrandedDNA, ProtozoanDrug ResistanceEvolution, MolecularGenome, ProtozoanHost-Parasite InteractionsHumansMalaria, FalciparumPlasmodium falciparumAntimalarialsDNA, Protozoan

Identifiers

PMID25184562
PMCPMC4187680

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.