Evidence map›Paper›PMID 20181722›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

TAF1 differentially enhances androgen receptor transcriptional activity via its N-terminal kinase and ubiquitin-activating and -conjugating domains.

Peyman Tavassoli, Latif A Wafa, Helen Cheng, Amina Zoubeidi, Ladan Fazli, Martin Gleave, Robert Snoek, Paul S Rennie

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Polyglutamine expansion induced dynamic misfolding of androgen receptor.Protein science : a publication of the Protein Society · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. The roles of TAF1 in neuroscience and beyond.Royal Society open science · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Long Noncoding RNAMolecular and cellular biology · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  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

8 authors at 1 institution in 1 country.

Peyman TavassoliDepartment of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Latif A Wafa
Helen Cheng
Amina Zoubeidi
Ladan Fazli
Martin Gleave
Robert Snoek
Paul S Rennie
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant expression of androgen receptor (AR) coregulators has been linked to progression of prostate cancers to castration resistance. Using the repressed transactivator yeast two-hybrid system, we found that TATA binding protein-associated factor 1 (TAF1) interacted with the AR. In tissue microarrays, TAF1 was shown to steadily increase with duration of neoadjuvant androgen withdrawal and with progression to castration resistance. Glutathione S-transferase pulldown assays established that TAF1 bound through its acetylation and ubiquitin-activating/conjugating domains (E1/E2) directly to the AR N terminus. Coimmunoprecipitation and ChIP assays revealed colocalization of TAF1 and AR on the prostate-specific antigen promoter/enhancer in prostate cancer cells. With respect to modulation of AR activity, overexpression of TAF1 enhanced AR activity severalfold, whereas small interfering RNA knockdown of TAF1 significantly decreased AR transactivation. Although full-length TAF1 showed enhancement of both AR and some generic gene transcriptional activity, selective AR coactivator activity by TAF1 was demonstrated in transactivation experiments using cloned N-terminal kinase and E1/E2 functional domains. In keeping with AR coactivation by the ubiquitin-activating and -conjugating domain, TAF1 was found to greatly increase the cellular amount of polyubiquitinated AR. In conclusion, our results indicate that increased TAF1 expression is associated with progression of human prostate cancers to the lethal castration-resistant state. Because TAF1 is a coactivator of AR that binds and enhances AR transcriptional activity, its overexpression could be part of a compensatory mechanism adapted by cancer cells to overcome reduced levels of circulating androgens.

Indexed as

Blotting, WesternCell Line, TumorHistone AcetyltransferasesHumansImmunoprecipitationIn Vitro TechniquesMaleProstatic NeoplasmsProtein BindingReceptors, AndrogenRNA, Small InterferingTATA-Binding Protein Associated FactorsTranscriptional ActivationTranscription Factor TFIIDTwo-Hybrid System TechniquesAR protein, humanHistone AcetyltransferasesReceptors, AndrogenRNA, Small InterferingTATA-binding protein associated factor 250 kDaTATA-Binding Protein Associated FactorsTranscription Factor TFIID

Identifiers

PMID20181722
PMCPMC5417532
OpenAlexW1998867125

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.