Evidence map›Paper›PMID 12502878›Full record

ArticleJournal of virology2003

The high-risk human papillomavirus type 16 E6 counters the GAP function of E6TP1 toward small Rap G proteins.

Latika Singh, Qingshen Gao, Ajay Kumar, Takaya Gotoh, David E Wazer, Hamid Band, Larry A Feig, Vimla Band

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Rap2B GTPase: structure, functions, and regulation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  6. Review
  7. Article
  8. Article
  9. Oncogenes and RNA splicing of human tumor viruses.Emerging microbes & infections · 2014
    Review
  10. Article
  11. Inhibitory effects of Rap1GAP overexpression on proliferation and migration of endothelial cells via ERK and Akt pathways.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2011
    Article
  12. Viral oncogenes, noncoding RNAs, and RNA splicing in human tumor viruses.International journal of biological sciences · 2010
    Review
  13. Review
  14. Human papilloma virus (HPV) and host cellular interactions.Pathology oncology research : POR · 2008
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

8 authors at 2 institutions in 1 country.

Latika SinghDivision of Radiation and Cancer Biology, Department of Radiation Oncology, New England Medical Center, Boston, Massachusetts 02111, USA.
Qingshen Gao
Ajay Kumar
Takaya Gotoh
David E Wazer
Hamid Band
Larry A Feig
Vimla Band
Tufts University · USBrigham and Women's Hospital · US

Funding

TYROSINE KINASE REGULATION VIA PROTEIN DEGRADATIONR01CA087986 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2000 to 2015
$4.2M
THE ROLE OF A NOVEL GAP IN EPITHELIAL ONCOGENESISR01CA081076 · NCI · TUFTS MEDICAL CENTER · PI BAND, VIMLA · 1999 to 2003
$988k
FUNCTIONAL DISSECTION OF CBLS TRANSFORMING DOMAINR01CA076118 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI BAND, HAMID · 1998 to 2002
$713k
HUMAN MAMMARY EPITHELIAL CELL IMMORTALIZATIONR01CA070195 · NCI · TUFTS MEDICAL CENTER · PI BAND, VIMLA · 1998 to 2002
$706k
REGULATING TYROSINE KINASE SIGNALS IN BREAST CANCERR01CA075075 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI BAND, HAMID · 1997 to 2001
$508k
NCI NIH HHS CA70195NCI NIH HHS CA75075NCI NIH HHS CA76118NCI NIH HHS CA81076NCI NIH HHS CA87986NCI NIH HHS R01 CA081076NCI NIH HHS R01 CA087986
6 · The paper itself

Abstract

We have recently identified E6TP1 (E6-targeted protein 1) as a novel high-risk human papillomavirus type 16 (HPV16) E6-binding protein. Importantly, mutational analysis of E6 revealed a strong correlation between the transforming activity and its abilities to bind and target E6TP1 for ubiquitin-mediated degradation. As a region within E6TP1 has high homology with GAP domains of known and putative Rap GTPase-activating proteins (GAPs), these results raised the possibility that HPV E6 may alter the Rap small-G-protein signaling pathway. Using two different approaches, we now demonstrate that human E6TP1 exhibits GAP activity for Rap1 and Rap2, confirming recent findings that a closely related rat homologue exhibits Rap-specific GAP activity. Using mutational analysis, we localize the GAP activity to residues 240 to 945 of E6TP1. Significantly, we demonstrate that coexpression of HPV16 E6, by promoting the degradation of E6TP1, enhances the GTP loading of Rap. These results support a role of Rap small-G-protein pathway in E6-mediated oncogenesis.

Indexed as

Repressor ProteinsCell LineGTPase-Activating ProteinsHumansOncogene Proteins, Viralrap GTP-Binding ProteinsE6 protein, Human papillomavirus type 16E6-target protein 1GTPase-Activating ProteinsOncogene Proteins, Viralrap GTP-Binding ProteinsRepressor Proteins

Identifiers

PMID12502878
PMCPMC140801
OpenAlexW2062604072

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.