Evidence map›Paper›PMID 38389037›Full record

ArticleClinical proteomics2024

Kinome and phosphoproteome reprogramming underlies the aberrant immune responses in critically ill COVID-19 patients.

Tomonori Kaneko, Sally Ezra, Rober Abdo, Courtney Voss, Shanshan Zhong, Xuguang Liu, Owen Hovey, Marat Slessarev, Logan Robert Van Nynatten, Mingliang Ye and 2 more

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical proteomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

Tomonori KanekoDepartments of Biochemistry, Western University, London, ON, N6A 5C1, Canada.
Sally Ezra *Departments of Biochemistry, Western University, London, ON, N6A 5C1, Canada.
Rober Abdo *Department of Pathology and Laboratory Medicine, Western University, London, Canada.
Courtney Voss *Departments of Biochemistry, Western University, London, ON, N6A 5C1, Canada.
Shanshan ZhongDepartments of Biochemistry, Western University, London, ON, N6A 5C1, Canada.
Xuguang LiuDepartments of Biochemistry, Western University, London, ON, N6A 5C1, Canada.
Owen HoveyDepartments of Biochemistry, Western University, London, ON, N6A 5C1, Canada.
Marat SlessarevDepartments of Medicine and Pediatrics, Western University, London, Canada.
Logan Robert Van NynattenDepartments of Medicine and Pediatrics, Western University, London, Canada.
Mingliang YeCAS Key Laboratory of Separation Sciences for Analytical Chemistry, National Chromatographic R&A Center, Dalian Institute of Chemical Physics, Chinese Academy of Sciences (CAS), Dalian, 116023, China.
Douglas D FraserDepartments of Medicine and Pediatrics, Western University, London, Canada.
Shawn Shun-Cheng LiDepartments of Biochemistry, Western University, London, ON, N6A 5C1, Canada. sli@uwo.ca.
Western University · CAChinese Academy of Sciences · CNLawson Health Research Institute · CA

Funding

Ontario Research Fund COVID-19 Rapid Research Fund
6 · The paper itself

Abstract

SARS-CoV-2 infection triggers extensive host immune reactions, leading to severe diseases in certain individuals. However, the molecular basis underlying the excessive yet non-productive immune responses in severe COVID-19 remains incompletely understood. In this study, we conducted a comprehensive analysis of the peripheral blood mononuclear cell (PBMC) proteome and phosphoproteome in sepsis patients positive or negative for SARS-CoV-2 infection, as well as healthy subjects, using quantitative mass spectrometry. Our findings demonstrate dynamic changes in the COVID-19 PBMC proteome and phosphoproteome during disease progression, with distinctive protein or phosphoprotein signatures capable of distinguishing longitudinal disease states. Furthermore, SARS-CoV-2 infection induces a global reprogramming of the kinome and phosphoproteome, resulting in defective adaptive immune response mediated by the B and T lymphocytes, compromised innate immune responses involving the SIGLEC and SLAM family of immunoreceptors, and excessive cytokine-JAK-STAT signaling. In addition to uncovering host proteome and phosphoproteome aberrations caused by SARS-CoV-2, our work recapitulates several reported therapeutic targets for COVID-19 and identified numerous new candidates, including the kinases PKG1, CK2, ROCK1/2, GRK2, SYK, JAK2/3, TYK2, DNA-PK, PKCδ, and the cytokine IL-12.

Indexed as

Antibody responseCOVID-19CytokineImmune regulationKinome reprogrammingMass spectrometryPhosphoproteomeProteomeSARS-CoV-2Tandem mass tag

Identifiers

PMID38389037
PMCPMC10882830
OpenAlexW4392041498

What OpenQuestion 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 OpenQuestion graph.