Evidence map›Paper›PMID 16103197›Full record

ArticleJournal of virology2005

Human cytomegalovirus IE1-72 activates ataxia telangiectasia mutated kinase and a p53/p21-mediated growth arrest response.

Jonathan P Castillo, Fiona M Frame, Harry A Rogoff, Mary T Pickering, Andrew D Yurochko, Timothy F Kowalik

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 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.2field-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

49 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. [Mechanism and significance of cell senescence induced by viral infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Overview of Human Cytomegalovirus Pathogenesis.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Early Nuclear Events after Herpesviral Infection.Journal of clinical medicine · 2019
    Review
  16. Human cytomegalovirus glycoprotein B variants affect viral entry, cell fusion, and genome stability.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  17. Review
  18. Article
  19. 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

6 authors at 2 institutions in 1 country.

Jonathan P CastilloProgram in Immunology and Virology, University of Massachusetts Medical School, Worcester, 01655, USA.
Fiona M Frame
Harry A Rogoff
Mary T Pickering
Andrew D Yurochko
Timothy F Kowalik
University of Massachusetts Chan Medical School · USLouisiana State University Health Sciences Center Shreveport · US

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
Analysis of HCMV Infection of Monocytes and MacrophagesR01AI056077 · NIAID · LOUISIANA STATE UNIV HSC SHREVEPORT · PI YUROCHKO, ANDREW D · 2004 to 2020
$4.7M
E2F AND APOPTOSISR01CA086038 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KOWALIK, TIMOTHY F · 2000 to 2004
$1.4M
HUMAN CYTOMEGALOVIRUS AND CELL PROLIFERATION CONTROLF31HL010334 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CASTILLO, JONATHAN P · 2000 to 2002
$53k
NCI NIH HHS CA86038NCI NIH HHS R01 CA086038NHLBI NIH HHS F31 HL010334NHLBI NIH HHS HL 10334-01NIAID NIH HHS AI56077NIAID NIH HHS R01 AI056077NIDDK NIH HHS DK32520NIDDK NIH HHS P30 DK032520
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) encodes several proteins that can modulate components of the cell cycle machinery. The UL123 gene product, IE1-72, binds the Rb-related, p107 protein and relieves its repression of E2F-responsive promoters; however, it is unable to induce quiescent cells to enter S phase in wild-type (p53(+/+)) cells. IE1-72 also induces p53 accumulation through an unknown mechanism. We present here evidence suggesting that IE1-72 may activate the p53 pathway by increasing the levels of p19(Arf) and by inducing the phosphorylation of p53 at Ser15. Phosphorylation of this residue by IE1-72 expression alone or HCMV infection is found to be dependent on the ataxia-telangiectasia mutated kinase. IE2-86 expression leads to p53 phosphorylation and may contribute to this phenotype in HCMV-infected cells. We also found that IE1-72 promotes p53 nuclear accumulation by abrogating p53 nuclear shuttling. These events result in the stimulation of p53 activity, leading to a p53- and p21-dependent inhibition of cell cycle progression from G(1) to S phase in cells transiently expressing IE1-72. Thus, like many of the small DNA tumor viruses, the first protein expressed upon HCMV infection activates a p53 response by the host cell.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCell CycleCell Cycle ProteinsCell LineCyclin-Dependent Kinase Inhibitor p21CytomegalovirusDNA-Binding ProteinsFibroblastsG1 PhaseImmediate-Early ProteinsPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor ProteinsViral ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsIE1 protein, cytomegalovirusImmediate-Early ProteinsPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor ProteinsViral Proteins

Identifiers

PMID16103197
PMCPMC1193638
OpenAlexW2103487477

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.