Evidence map›Paper›PMID 24523872›Full record

ArticlePloS one2014

BRK targets Dok1 for ubiquitin-mediated proteasomal degradation to promote cell proliferation and migration.

Sayem Miah, Raghuveera Kumar Goel, Chenlu Dai, Natasha Kalra, Erika Beaton-Brown, Edward T Bagu, Keith Bonham, Kiven E Lukong

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. DOKing tumor progression in ccRCC.Journal of Cancer · 2024
    Article
  3. Review
  4. Review
  5. TRAF3: Guardian of T lymphocyte functions.Frontiers in immunology · 2023
    Review
  6. Article
  7. Article
  8. Targeting protein tyrosine kinase 6 in cancer.Biochimica et biophysica acta. Reviews on cancer · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Sayem MiahDepartment of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Raghuveera Kumar GoelDepartment of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Chenlu DaiDepartment of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Natasha KalraDepartment of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Erika Beaton-BrownDepartment of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada ; Cancer Research Unit, Health Research Division, Saskatchewan Cancer Agency, and Division of Oncology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Edward T BaguDepartment of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada ; Cancer Research Unit, Health Research Division, Saskatchewan Cancer Agency, and Division of Oncology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Keith BonhamDepartment of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada ; Cancer Research Unit, Health Research Division, Saskatchewan Cancer Agency, and Division of Oncology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Kiven E LukongDepartment of Biochemistry, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
University of Saskatchewan · CASaskatchewan Cancer Agency · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast tumor kinase (BRK), also known as protein tyrosine kinase 6 (PTK6), is a non-receptor tyrosine kinase overexpressed in more that 60% of human breast carcinomas. The overexpression of BRK has been shown to sensitize mammary epithelial cells to mitogenic signaling and to promote cell proliferation and tumor formation. The molecular mechanisms of BRK have been unveiled by the identification and characterization of BRK target proteins. Downstream of tyrosine kinases 1 or Dok1 is a scaffolding protein and a substrate of several tyrosine kinases. Herein we show that BRK interacts with and phosphorylates Dok1 specifically on Y362. We demonstrate that this phosphorylation by BRK significantly downregulates Dok1 in a ubiquitin-proteasome-mediated mechanism. Together, these results suggest a novel mechanism of action of BRK in the promotion of tumor formation, which involves the targeting of tumor suppressor Dok1 for degradation through the ubiquitin proteasomal pathway.

Indexed as

Gene Expression Regulation, NeoplasticBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDNA-Binding ProteinsFemaleGenes, Tumor SuppressorGreen Fluorescent ProteinsHEK293 CellsHumansNeoplasm ProteinsPhosphoproteinsPhosphorylationProteasome Endopeptidase ComplexProtein-Tyrosine KinasesDNA-Binding ProteinsDOK1 protein, humanGreen Fluorescent ProteinsNeoplasm ProteinsPhosphoproteinsProteasome Endopeptidase ComplexProtein-Tyrosine KinasesPTK6 protein, humanRNA-Binding Proteins

Identifiers

PMID24523872
PMCPMC3921129
OpenAlexW1965395090

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.