Evidence map›Paper›PMID 16847754›Full record

ReviewCellular & molecular biology letters2006

Degradation and beyond: control of androgen receptor activity by the proteasome system.

Tomasz Jaworski

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular & molecular biology letters, 2006. 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
0.8field-weighted citation impact, top 30% 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, 42 citations in OpenAlex.

  1. Review
  2. Review
  3. Functional roles of E3 ubiquitin ligases in prostate cancer.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
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  8. Review
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  14. Review
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  17. Androgen receptor W741C and T877A mutations in AIDL cells, an androgen-independent subline of prostate cancer LNCaP cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011
    Article
  18. Article
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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

1 author at 1 institution in 1 country.

Tomasz JaworskiDepartment of Cellular Biochemistry, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland. tomasz_jaworski@poczta.onet.pl
Instytut Biologii Doświadczalnej im. Marcelego Nenckiego · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The androgen receptor (AR) is a transcription factor belonging to the family of nuclear receptors which mediates the action of androgens in the development of urogenital structures. AR expression is regulated post-translationally by the ubiquitin/proteasome system. This regulation involves more complex mechanisms than typical degradation. The ubiquitin/proteasome system may regulate AR via mechanisms that do not engage in receptor turnover. Given the critical role of AR in sexual development, this complex regulation is especially important. Deregulation of AR signalling may be a causal factor in prostate cancer development. AR is the main target in prostate cancer therapies. Due to the critical role of the ubiquitin/proteasome system in AR regulation, current research suggests that targeting AR degradation is a promising approach.

Indexed as

AnimalsHumansLigandsMaleProstatic NeoplasmsProteasome Endopeptidase ComplexReceptors, AndrogenTranscription, GeneticUbiquitinLigandsProteasome Endopeptidase ComplexReceptors, AndrogenUbiquitin

Identifiers

PMID16847754
PMCPMC6275697
OpenAlexW2029907345

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.