Evidence map›Paper›PMID 18583474›Full record

ArticleThe Journal of endocrinology2008

Identification and functional analysis of SKA2 interaction with the glucocorticoid receptor.

Lisa Rice, Charlotte E Waters, Jennifer Eccles, Helen Garside, Paula Sommer, Paul Kay, Fiona H Blackhall, Leo Zeef, Brian Telfer, Ian Stratford and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 28% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. SKA2 enhances stress-related glucocorticoid receptor signaling through FKBP4-FKBP5 interactions in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Molecular Changes Associated with Suicide.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. The Role of Epigenetic Dysregulation in Suicidal Behaviors.Current topics in behavioral neurosciences · 2020
    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

15 authors at 1 institution in 1 country.

Lisa RiceFaculty of Medical and Human Sciences, School of Medicine, University of Manchester, Manchester M13 9PT, UK.
Charlotte E Waters
Jennifer Eccles
Helen Garside
Paula Sommer
Paul Kay
Fiona H Blackhall
Leo Zeef
Brian Telfer
Ian Stratford
Rob Clarke
Dave Singh
Adam Stevens
Anne White
David W Ray
University of Manchester · GB

Funding

Biotechnology and Biological Sciences Research CouncilBreast Cancer Now 2006MAYSF01Wellcome Trust
6 · The paper itself

Abstract

Glucocorticoid (GC) receptors (GRs) have profound anti-survival effects on human small cell lung cancer (SCLC). To explore the basis of these effects, protein partners for GRs were sought using a yeast two-hybrid screen. We discovered a novel gene, FAM33A, subsequently identified as a SKA1 partner and involved in mitosis, and so renamed Ska2. We produced an anti-peptide antibody that specifically recognized full-length human SKA2 to measure expression in human cell lines and tissues. There was a wide variation in expression across multiple cell lines, but none was detected in the liver cell line HepG2. A xenograft model of human SCLC had intense staining and archival tissue revealed SKA2 in several human lung and breast tumours. SKA2 was found in the cytoplasm, where it co-localized with GR, but nuclear expression of SKA2 was seen in breast tumours. SKA2 overexpression increased GC transactivation in HepG2 cells while SKA2 knockdown in A549 human lung epithelial cells decreased transactivation and prevented dexamethasone inhibition of proliferation. GC treatment decreased SKA2 protein levels in A549 cells, as did Staurosporine, phorbol ester and trichostatin A; all agents that inhibit cell proliferation. Overexpression of SKA2 potentiated the proliferative response to IGF-I exposure, and knockdown with shRNA caused cells to arrest in mitosis. SKA2 has recently been identified in HeLa S3 cells as part of a complex, which is critical for spindle checkpoint silencing and exit from mitosis. Our new data show involvement in cell proliferation and GC signalling, with implications for understanding how GCs impact on cell fate.

Indexed as

3T3-L1 CellsAmino Acid SequenceAnimalsBlotting, WesternBreast NeoplasmsCell LineCell Line, TumorCell ProliferationChromosomal Proteins, Non-HistoneHumansImmunohistochemistryIn Vitro TechniquesLung NeoplasmsMiceMolecular Sequence DataOligonucleotide Array Sequence AnalysisChromosomal Proteins, Non-HistoneReceptors, GlucocorticoidRNA, Small InterferingSKA2 protein, human

Identifiers

PMID18583474
PMCPMC2518725
OpenAlexW2039808529

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.