Evidence map›Paper›PMID 12096338›Full record

ArticleOncogene2002

Adenovirus encoding HIV-1 Vpr activates caspase 9 and induces apoptotic cell death in both p53 positive and negative human tumor cell lines.

Karuppiah Muthumani, Donghui Zhang, Daniel S Hwang, Sagar Kudchodkar, Nathanael S Dayes, Brijal M Desai, Afshan S Malik, Joo-Sung Yang, Michael A Chattergoon, Henry C Maguire and 1 more

Abstract read
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In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. HIV-1 viral protein R downregulates Ebp1 and stabilizes p53 in glioblastoma U87MG cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
    Article
  9. Article
  10. T-Cell Signaling in HIV-1 Infection.The open virology journal · 2013
    Article
  11. Article
  12. Article
  13. Vpr-host interactions during HIV-1 viral life cycle.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

11 authors at 2 institutions in 1 country.

Karuppiah MuthumaniDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, PA 19104, USA.
Donghui Zhang
Daniel S Hwang
Sagar Kudchodkar
Nathanael S Dayes
Brijal M Desai
Afshan S Malik
Joo-Sung Yang
Michael A Chattergoon
Henry C Maguire
David B Weiner
University of Pennsylvania · USGlobal Viral · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The targeted delivery of genes whose products arrest the cell cycle and/or induce apoptosis represent an important tool for the understanding and controlling forms of unregulated cell growth. The vpr gene product of HIV-1 has been reported to interfere with cell growth and induce apoptosis, but the mechanism of its action is not clearly understood. In order to study these important properties of Vpr, we created a recombinant adenovirus H5.010CMV-vpr (adCMV-vpr) as a tool to deliver the vpr gene to various cell lines to examine its biology. Vpr protein expression was confirmed by Western blot analysis in adCMV-vpr infected cells. We tested the effects of adCMV-vpr on cell growth of several tumor cell lines. Infection of both p53 positive and p53 deficient tumor cell lines with adCMV-vpr resulted in dramatic induction of cell death in short-term assays. We observed that apoptosis was induced through the mitochondrial pathway as we observed changes in the cytochrome c content accompanied by caspase 9 activation. As Bcl-2 is reported to interfere with apoptosis through the mitochondrial pathway, we examined the effect of adCMV-vpr in Bcl-2 over expressing cell lines. We observed that Bcl-2 overexpression does not inhibit adCMV-vpr induced apoptosis. The properties of adCMV-vpr inducing apoptosis through caspase 9 in a p53 pathway independent manner suggest that this is an important reagent. Such a vector may give insight into approaches designed to limit the growth of pathogenic human cells.

Indexed as

ApoptosisAdenoviridaeBlotting, WesternCaspase 9CaspasesCell CycleCell SizeCell SurvivalEnzyme ActivationFlow CytometryGene DeletionGene ExpressionGene Products, vprGenetic VectorsHeLa CellsHumansCASP9 protein, humanCaspase 9CaspasesGene Products, vprProto-Oncogene Proteins c-bcl-2Tumor Suppressor Protein p53

Identifiers

PMID12096338
OpenAlexW2008489945

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.