Evidence map›Paper›PMID 16189003›Full record

ArticleJournal of virology2005

Induction and utilization of an ATM signaling pathway by polyomavirus.

Jean Dahl, John You, Thomas L Benjamin

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

85 citing papers in PubMed, 127 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. SARS-CoV-2 and the DNA damage response.The Journal of general virology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Possible Beneficial Actions of Caffeine in SARS-CoV-2.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

25 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 at 1 institution in 1 country.

Jean DahlDepartment of Pathology, Harvard Medical School, Boston, MA 02115, USA.
John You
Thomas L Benjamin
Harvard University · US

Funding

POLYOMA HOST INTERACTIONS LEADING TO TUMOR DEVELOPMENTR01CA090992 · NCI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BENJAMIN, THOMAS LIVINGSTON · 2001 to 2005
$3.7M
NCI NIH HHS R01 CA090992NCI NIH HHS R01 CA90992
6 · The paper itself

Abstract

Progression from G(1) to S is essential for polyomavirus DNA replication and depends on the interaction of large T with the retinoblastoma gene product pRb. This virus-induced replication pathway is accompanied by p53 activation resembling a DNA damage response (12). We sought to determine whether this pathway depends in part on activation of the ATM (ataxia telangiectasia mutated) kinase and whether the virus gains advantages from this pathway beyond that of entry into S. We show that polyomavirus infection activates the S- and G(2)-phase checkpoints in primary as well as established mouse cells. Infected cells undergo a prolonged S phase compared to uninfected serum-stimulated cells and show no evidence of a G(2)-->M transition before lytic death ensues. Infection is accompanied by increases in ATM activity in vitro and in the level of ATM-S1981-P in vivo. The incubation of infected cells with caffeine, a known ATM inhibitor, did not block entry into S but reduced the rate of viral compared to cellular DNA synthesis. Importantly, caffeine lowered the yields of viral DNA an average of 3- to 6-fold and those of infectious virus by as much as 10-fold. Virus yields were 10-fold lower in ATM (-/-) p53(-/-) than in ATM(+/+) p53(-/-) mouse embryo fibroblasts, indicating a p53-independent role of ATM in productive infection. Replacement of the normal SMC1 (structural maintenance of chromosomes, or cohesin) protein, a critical ATM substrate in the DNA repair pathway, with its phosphorylation mutant SMC1(S957AS966A) also lowered virus yields by roughly 90%. We suggest that polyomavirus activates and utilizes a component(s) of an ATM pathway of DNA repair to prolong S phase and aid its own replication.

Indexed as

Signal TransductionAnimalsAtaxia Telangiectasia Mutated ProteinsBALB 3T3 CellsCell CycleCell Cycle ProteinsDNA-Binding ProteinsMicePhosphatidylinositol 3-KinasesPolyomavirusPolyomavirus InfectionsProtein Serine-Threonine KinasesTumor Suppressor ProteinsTumor Virus InfectionsAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID16189003
PMCPMC1235815
OpenAlexW2146912213

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.