Evidence map›Paper›PMID 15140963›Full record

ArticleJournal of virology2004

Murine coronavirus replication induces cell cycle arrest in G0/G1 phase.

Chun-Jen Chen, Shinji Makino

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

69 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Roles of p53-Mediated Host-Virus Interaction in Coronavirus Infection.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Deleterious Effects of SARS-CoV-2 Infection on Human Pancreatic Cells.Frontiers in cellular and infection microbiology · 2021
    Article
  20. Article

9 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

2 authors at 1 institution in 1 country.

Chun-Jen ChenDepartment of Microbiology and Immunology, The University of Texas Medical Branch at Galveston, MRB 4.146, 301 University Blvd., Galveston, TX 77555-1019, USA.
Shinji Makino
The University of Texas Medical Branch at Galveston · US

Funding

MOLECULAR STUDIES OF CORONAVIRUS REPLICATIONR01AI029984 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI MAKINO, SHINJI · 1990 to 2006
$1.5M
Molecular Studies of Coronavirus ReplicationR21AI029984 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI MAKINO, SHINJI · 2001 to 2001
$261k
NIAID NIH HHS AI29984NIAID NIH HHS R01 AI029984NIAID NIH HHS R21 AI029984
6 · The paper itself

Abstract

Mouse hepatitis virus (MHV) replication in actively growing DBT and 17Cl-1 cells resulted in the inhibition of host cellular DNA synthesis and the accumulation of infected cells in the G(0)/G(1) phase of the cell cycle. UV-irradiated MHV failed to inhibit host cellular DNA synthesis. MHV infection in quiescent 17Cl-1 cells that had been synchronized in the G(0) phase by serum deprivation prevented infected cells from entering the S phase after serum stimulation. MHV replication inhibited hyperphosphorylation of the retinoblastoma protein (pRb), the event that is necessary for cell cycle progression through late G(1) and into the S phase. While the amounts of the cellular cyclin-dependent kinase (Cdk) inhibitors p21(Cip1), p27(Kip1), and p16(INK4a) did not change in infected cells, MHV infection in asynchronous cultures induced a clear reduction in the amounts of Cdk4 and G(1) cyclins (cyclins D1, D2, D3, and E) in both DBT and 17Cl-1 cells and a reduction in Cdk6 levels in 17Cl-1 cells. Infection also resulted in a decrease in Cdk2 activity in both cell lines. MHV infection in quiescent 17Cl-1 cells prevented normal increases in Cdk4, Cdk6, cyclin D1, and cyclin D3 levels after serum stimulation. The amounts of cyclin D2 and cyclin E were not increased significantly after serum stimulation in mock-infected cells, whereas they were decreased in MHV-infected cells, suggesting the possibility that MHV infection may induce cyclin D2 and cyclin E degradation. Our data suggested that a reduction in the amounts of G(1) cyclin-Cdk complexes in MHV-infected cells led to a reduction in Cdk activities and insufficient hyperphosphorylation of pRb, resulting in inhibition of the cell cycle in the G(0)/G(1) phase.

Indexed as

G1 PhaseResting Phase, Cell CycleVirus ReplicationAnimalsCDC2-CDC28 KinasesCell DivisionCyclin-Dependent Kinase 2DNAMiceMurine hepatitis virusPhosphorylationRetinoblastoma ProteinCDC2-CDC28 KinasesCdk2 protein, mouseCyclin-Dependent Kinase 2DNARetinoblastoma Protein

Identifiers

PMID15140963
PMCPMC415820
OpenAlexW2151089483

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.