Evidence map›Paper›PMID 24424504›Full record

ReviewEndocrine-related cancer2014

Androgen receptor phosphorylation: biological context and functional consequences.

Yulia Koryakina, Huy Q Ta, Daniel Gioeli

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine-related cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
9.2field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. The Ser434PheThe application of clinical genetics · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Androgen Receptor in Hormone Receptor-Positive Breast Cancer.International journal of molecular sciences · 2023
    Review
  20. Article

10 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution.

Yulia KoryakinaDepartment of MicrobiologyImmunology, and Cancer BiologyUVA Cancer CenterUniversity of Virginia, PO Box 800734, Charlottesville, Virginia 22908, USA.
Huy Q TaDepartment of MicrobiologyImmunology, and Cancer BiologyUVA Cancer CenterUniversity of Virginia, PO Box 800734, Charlottesville, Virginia 22908, USA.
Daniel GioeliDepartment of MicrobiologyImmunology, and Cancer BiologyUVA Cancer CenterUniversity of Virginia, PO Box 800734, Charlottesville, Virginia 22908, USADepartment of MicrobiologyImmunology, and Cancer BiologyUVA Cancer CenterUniversity of Virginia, PO Box 800734, Charlottesville, Virginia 22908, USA DGG3F@VIRGINIA.EDU.
University of Virginia Cancer Center

Funding

Checkpoint Signaling and Androgen Receptor Function in Prostate CancerR01CA178338 · NCI · UNIVERSITY OF VIRGINIA · PI GIOELI, DANIEL G · 2014 to 2018
$1.6M
Role of Androgen Receptor Phosphorylation in Prostate CancerR01CA124706 · NCI · UNIVERSITY OF VIRGINIA · PI GIOELI, DANIEL G · 2008 to 2012
$1.6M
NCI NIH HHS R01 CA124706NCI NIH HHS R01 CA178338
6 · The paper itself

Abstract

The androgen receptor (AR) is a ligand-regulated transcription factor that belongs to the family of nuclear receptors. In addition to regulation by steroid, the AR is also regulated by post-translational modifications generated by signal transduction pathways. Thus, the AR functions not only as a transcription factor but also as a node that integrates multiple extracellular signals. The AR plays an important role in many diseases, including complete androgen insensitivity syndrome, spinal bulbar muscular atrophy, prostate and breast cancer, etc. In the case of prostate cancer, dependence on AR signaling has been exploited for therapeutic intervention for decades. However, the effectiveness of these therapies is limited in advanced disease due to restoration of AR signaling. Greater understanding of the molecular mechanisms involved in AR action will enable the development of improved therapeutics to treat the wide range of AR-dependent diseases. The AR is subject to regulation by a number of kinases through post-translational modifications on serine, threonine, and tyrosine residues. In this paper, we review the AR phosphorylation sites, the kinases responsible for these phosphorylations, as well as the biological context and the functional consequences of these phosphorylations. Finally, what is known about the state of AR phosphorylation in clinical samples is discussed.

Indexed as

AnimalsHumansPhosphorylationProtein KinasesProtein Structure, TertiaryReceptors, AndrogenProtein KinasesReceptors, Androgenandrogen receptorcell signalinggene transcriptiongrowth factorprostate

Identifiers

PMID24424504
PMCPMC4437516
OpenAlexW2165846310

What OpenQuestion holds

Textmetadata
LicenceTDM
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.