Evidence map›Paper›PMID 26190101›Full record

ArticleCell reports2015

Genome-wide Analysis of Host-Plasmodium yoelii Interactions Reveals Regulators of the Type I Interferon Response.

Jian Wu, Baowei Cai, Wenxiang Sun, Ruili Huang, Xueqiao Liu, Meng Lin, Sittiporn Pattaradilokrat, Scott Martin, Yanwei Qi, Sethu C Nair and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. NAD activates olfactory receptor 1386 to regulate type I interferon responses inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Malaria Genomics, Vaccine Development, and Microbiome.Pathogens (Basel, Switzerland) · 2023
    Review
  6. Review
  7. Forward Genetics in Apicomplexa Biology: The Host Side of the Story.Frontiers in cellular and infection microbiology · 2022
    Review
  8. Article
  9. RTP4 inhibits IFN-I response and enhances experimental cerebral malaria and neuropathology.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. The E3 ubiquitin ligase MARCH1 regulates antimalaria immunity through interferon signaling and T cell activation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Article
  12. Article
  13. Host-Malaria Parasite Interactions and Impacts on Mutual Evolution.Frontiers in cellular and infection microbiology · 2020
    Review
  14. Review
  15. Clinical microbiology reviews · 2019
    Review
  16. ELF4 facilitates innate host defenses againstThe Journal of biological chemistry · 2019
    Article
  17. Article
  18. Article
  19. Protozoan Parasites and Type I IFNs.Frontiers in immunology · 2017
    Review
  20. Article
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

17 authors at 6 institutions in 3 countries.

Jian WuLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Baowei CaiState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, PRC; Center for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Wenxiang SunLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Ruili HuangNational Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Xueqiao LiuLaboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Meng LinCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Sittiporn PattaradilokratLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA; Department of Biology, Faculty of Science, Chulalongkorn University, Bangkok 10330, Thailand.
Scott MartinNational Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Yanwei QiLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA; State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, PRC.
Sethu C NairLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Silvia BollandLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Jeffrey I CohenLaboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Christopher P AustinNational Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Carole A LongLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Timothy G MyersGenomic Technologies Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA.
Rong-Fu WangCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA. Electronic address: rwang3@houstonmethodist.org.
Xin-Zhuan SuLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA; State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, PRC. Electronic address: xsu@niaid.nih.gov.
National Institutes of Health · USNational Center for Advancing Translational Sciences · USHouston Methodist · USNational Institute of Allergy and Infectious Diseases · USXiamen University · CNChulalongkorn University · TH

Funding

Infectious Diseases Research Technologies Core - BethesdaZICAI001051 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$226.1M
Genetic Modifiers Of Autoimmune Disease In FcgammaRIIB Mutant MiceZIAAI000912 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BOLLAND, SILVIA · 2009 to 2025
$27.0M
Malaria Parasite Sexual Development, Drug Resistance, and EvolutionZIAAI000892 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SU, XINZHUAN · 2009 to 2025
$23.3M
Host Immune Responses to Antigens of Malaria ParasitesZIAAI001020 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LONG, CAROLE · 2009 to 2025
$13.6M
Trans-NIH RNAi Facility (TNRF)ZICTR000041 · NCATS · NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES · PI CHENG, KEN · 2015 to 2025
$9.4M
Novel Strategies for Intervention of Inflammatory Diseases and Cancer - Research Supplement to R01-CA101795R01CA101795 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WANG, RONGFU · 2004 to 2022
$4.6M
The Role of CD4+ T Cells in Antitumor ImmunityR01CA090327 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI WANG, RONGFU · 2002 to 2013
$3.0M
Intramural NIH HHS ZIA AI000892NCI NIH HHS R01 CA090327NCI NIH HHS R01CA090327NCI NIH HHS R01 CA101795NCI NIH HHS R01CA101795
6 · The paper itself

Abstract

Invading pathogens trigger specific host responses, an understanding of which might identify genes that function in pathogen recognition and elimination. In this study, we performed trans-species expression quantitative trait locus (ts-eQTL) analysis using genotypes of the Plasmodium yoelii malaria parasite and phenotypes of mouse gene expression. We significantly linked 1,054 host genes to parasite genetic loci (LOD score ≥ 3.0). Using LOD score patterns, which produced results that differed from direct expression-level clustering, we grouped host genes that function in related pathways, allowing functional prediction of unknown genes. As a proof of principle, 14 of 15 randomly selected genes predicted to function in type I interferon (IFN-I) responses were experimentally validated using overexpression, small hairpin RNA knockdown, viral infection, and/or infection of knockout mice. This study demonstrates an effective strategy for studying gene function, establishes a functional gene database, and identifies regulators in IFN-I pathways.

Indexed as

AnimalsGenome, ProtozoanGenome-Wide Association StudyHost-Parasite InteractionsInterferon Type IMalariaMiceMice, Inbred C57BLPlasmodium yoeliiQuantitative Trait LociInterferon Type I

Identifiers

PMID26190101
PMCPMC4520759
OpenAlexW1573275207

What OpenQuestion holds

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Registered trials

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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.