Evidence map›Paper›PMID 37310920›Full record

ArticlePLoS biology2023

DYRK1A promotes viral entry of highly pathogenic human coronaviruses in a kinase-independent manner.

Madison S Strine, Wesley L Cai, Jin Wei, Mia Madel Alfajaro, Renata B Filler, Scott B Biering, Sylvia Sarnik, Ryan D Chow, Ajinkya Patil, Kasey S Cervantes and 11 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  5. Article
  6. Cell entry mechanisms of porcine enteric coronaviruses.The Journal of biological chemistry · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
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  20. Review
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

21 authors at 11 institutions in 2 countries.

Madison S StrineDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Wesley L CaiHillman Cancer Center, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.
Jin WeiDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Mia Madel AlfajaroDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Renata B FillerDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Scott B BieringDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California, Berkeley, Berkeley, California, United States of America.
Sylvia SarnikUniversity of Colorado Boulder, Boulder, Colorado, United States of America.
Ryan D ChowDepartment of Genetics, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Ajinkya PatilDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States of America.
Kasey S CervantesDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States of America.
Clayton K CollingsDepartment of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States of America.
Peter C DeWeirdtGenetic Perturbation Platform, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, United States of America.
Ruth E HannaGenetic Perturbation Platform, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, United States of America.
Kevin SchofieldDepartment of Chemistry and Biochemistry, College of Science, The University of Arizona, Tucson, Arizona, United States of America.
Christopher HulmeDepartment of Chemistry and Biochemistry, College of Science, The University of Arizona, Tucson, Arizona, United States of America.
Silvana KonermannDepartment of Biochemistry, Stanford University School of Medicine, Stanford, California, United States of America.
John G DoenchGenetic Perturbation Platform, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, United States of America.
Patrick D HsuArc Institute, Palo Alto, California, United States of America.
Cigall KadochDepartment of Genetics, Yale University School of Medicine, New Haven, Connecticut, United States of America.
Qin YanDepartment of Pathology, Yale School of Medicine, New Haven, Connecticut, United States of America.
Craig B WilenDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America.ORCID 0000-0003-2495-9403
Broad Institute · USYale University · USUniversity of Arizona · USYale Cancer Center · USChinese Academy of Sciences · CNHoward Hughes Medical Institute · USInnovative Genomics Institute · USPalo Alto Institute · USUniversity of California, Berkeley · USUniversity of Colorado Boulder · USUPMC Hillman Cancer Center · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
The role of tuft cells in norovirus pathogenesisR01AI148467 · NIAID · YALE UNIVERSITY · PI Craig Brian Wilen · 2020 to 2026
$3.9M
Role of virus-receptor interactions in determining norovirus tropism and pathogenesis in vivoK08AI128043 · NIAID · YALE UNIVERSITY · PI WILEN, CRAIG BRIAN · 2017 to 2021
$940k
NCATS NIH HHS UL1 TR001863NIAID NIH HHS K08 AI128043NIAID NIH HHS R01 AI148467
6 · The paper itself

Abstract

Identifying host genes essential for Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has the potential to reveal novel drug targets and further our understanding of Coronavirus Disease 2019 (COVID-19). We previously performed a genome-wide CRISPR/Cas9 screen to identify proviral host factors for highly pathogenic human coronaviruses. Few host factors were required by diverse coronaviruses across multiple cell types, but DYRK1A was one such exception. Although its role in coronavirus infection was previously undescribed, DYRK1A encodes Dual Specificity Tyrosine Phosphorylation Regulated Kinase 1A and is known to regulate cell proliferation and neuronal development. Here, we demonstrate that DYRK1A regulates ACE2 and DPP4 transcription independent of its catalytic kinase function to support SARS-CoV, SARS-CoV-2, and Middle East Respiratory Syndrome Coronavirus (MERS-CoV) entry. We show that DYRK1A promotes DNA accessibility at the ACE2 promoter and a putative distal enhancer, facilitating transcription and gene expression. Finally, we validate that the proviral activity of DYRK1A is conserved across species using cells of nonhuman primate and human origin. In summary, we report that DYRK1A is a novel regulator of ACE2 and DPP4 expression that may dictate susceptibility to multiple highly pathogenic human coronaviruses.

Indexed as

COVID-19Virus InternalizationAngiotensin-Converting Enzyme 2AnimalsDipeptidyl Peptidase 4Dyrk KinasesHumansMiddle East Respiratory Syndrome CoronavirusSARS-CoV-2Severe acute respiratory syndrome-related coronavirusAngiotensin-Converting Enzyme 2Dipeptidyl Peptidase 4Dyrk Kinases

Identifiers

PMID37310920
PMCPMC10263356
OpenAlexW4380537710

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.