Evidence map›Paper›PMID 14755242›Full record

ArticleOncogene2004

HIV-1 Tat increases cell survival in response to cisplatin by stimulating Rad51 gene expression.

Galina Chipitsyna, Dorota Slonina, Khwaja Siddiqui, Francesca Peruzzi, Tomasz Skorski, Krzysztof Reiss, Bassel E Sawaya, Kamel Khalili, Shohreh Amini

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Functional roles of HIV-1 Tat protein in the nucleus.Cellular and molecular life sciences : CMLS · 2016
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Activation of HIV-1 LTR by Rad51 in microglial cells.Cell cycle (Georgetown, Tex.) · 2010
    Article
  14. Review
  15. Review
  16. Article
  17. HIV-1 Tat and AIDS-associated cancer: targeting the cellular anti-cancer barrier?Journal of experimental & clinical cancer research : CR · 2008
    Review
  18. Article
  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

9 authors at 2 institutions in 1 country.

Galina ChipitsynaCenter for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, 1900 North 12th Street, 015-96, Philadelphia, PA 19122, USA.
Dorota Slonina
Khwaja Siddiqui
Francesca Peruzzi
Tomasz Skorski
Krzysztof Reiss
Bassel E Sawaya
Kamel Khalili
Shohreh Amini
Temple University · USUniversity of the Sciences · US

Funding

REGULATION OF HIV-1 GENE TRANSCRIPTION IN CNSR01NS040673 · NINDS · TEMPLE UNIVERSITY · PI SAWAYA, BASSEL E · 2000 to 2004
$1.6M
NINDS NIH HHS R01 NS040673
6 · The paper itself

Abstract

Tat is an early regulatory protein of human immunodeficiency virus type 1, which plays a central role in the pathogenesis of AIDS by stimulating transcription of the viral genome and impairing several important cellular pathways during the progression of the disease. Here, we investigated the effect of Tat on cell response to DNA damage. Our results indicate that Tat production causes a noticeable increase in the survival rate of PC12 cells upon their treatment with genotoxic agents. Single-cell gel electrophoresis studies revealed reduced DNA breakage in PC12-Tat cells upon cisplatin treatment relative to the control cells. Furthermore, cytogenetic data exhibited less chromosomal damage in Tat-producing cells after recovery from cisplatin treatment, corroborating electrophoretic data. Examination of several proteins involved in the control of DNA repair showed elevated levels of Rad51, a key regulator of homologous recombination in cells expressing Tat. On the other hand, the level of Ku70, one of the components of the nonhomologous end-joining repair pathway, was slightly decreased in cells expressing Tat. Using a fluorescence-based assay, we demonstrated that repair of DNA double-strand breaks via homologous recombination is increased in Tat-producing cells. The results from in vitro nonhomologous end-joining assay revealed a reduced ability of protein extract from PC12-Tat cells compared to PC12 cells in rejoining linearized DNA. These observations ascribe a new role for Tat in host genomic integrity, perhaps by affecting the expression of genes involved in DNA repair.

Indexed as

AnimalsAntigens, NuclearAntineoplastic AgentsBlotting, WesternCell SurvivalChromosome AberrationsCisplatinComet AssayDNA-Binding ProteinsDNA, ComplementaryDNA DamageDNA RepairGene Products, tatGenes, ReporterKu AutoantigenLuciferasesAntigens, NuclearAntineoplastic AgentsCisplatinDNA-Binding ProteinsDNA, ComplementaryGene Products, tatKu AutoantigenLuciferasesRad51 protein, ratRad51 RecombinaseXrcc6 protein, humanXrcc6 protein, rat

Identifiers

PMID14755242
OpenAlexW1970564926

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.