Evidence map›Paper›PMID 21795712›Full record

ArticleThe Journal of biological chemistry2011

RB1CC1 protein positively regulates transforming growth factor-beta signaling through the modulation of Arkadia E3 ubiquitin ligase activity.

Daizo Koinuma, Masahiko Shinozaki, Yoshiko Nagano, Hiroaki Ikushima, Kana Horiguchi, Kouichiro Goto, Tokuhiro Chano, Masao Saitoh, Takeshi Imamura, Kohei Miyazono and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Regulation of TGF-β Family Signaling by Inhibitory Smads.Cold Spring Harbor perspectives in biology · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Autophagy signal transduction by ATG proteins: from hierarchies to networks.Cellular and molecular life sciences : CMLS · 2015
    Review
  13. Article
  14. Robo1 modulates proliferation and neurogenesis in the developing neocortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

11 authors at 5 institutions in 1 country.

Daizo KoinumaDivision of Biochemistry, The Cancer Institute of the Japanese Foundation for Cancer Research, Koto-ku, Tokyo 135-8550, Japan.
Masahiko Shinozaki
Yoshiko Nagano
Hiroaki Ikushima
Kana Horiguchi
Kouichiro Goto
Tokuhiro Chano
Masao Saitoh
Takeshi Imamura
Kohei Miyazono
Keiji Miyazawa
The University of Tokyo · JPEhime University · JPJapanese Foundation For Cancer Research · JPShiga University of Medical Science · JPUniversity of Yamanashi · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) signaling is controlled by a variety of regulators, of which Smad7, c-Ski, and SnoN play a pivotal role in its negative regulation. Arkadia is a RING-type E3 ubiquitin ligase that targets these negative regulators for degradation to enhance TGF-β signaling. In the present study we identified a candidate human tumor suppressor gene product RB1CC1/FIP200 as a novel positive regulator of TGF-β signaling that functions as a substrate-selective cofactor of Arkadia. Overexpression of RB1CC1 enhanced TGF-β signaling, and knockdown of endogenous RB1CC1 attenuated TGF-β-induced expression of target genes as well as TGF-β-induced cytostasis. RB1CC1 down-regulated the protein levels of c-Ski but not SnoN by enhancing the activity of Arkadia E3 ligase toward c-Ski. Substrate selectivity is primarily attributable to the physical interaction of RB1CC1 with substrates, suggesting its role as a scaffold protein. RB1CC1 thus appears to play a unique role as a modulator of TGF-β signaling by restricting substrate specificity of Arkadia.

Indexed as

AnimalsAutophagy-Related ProteinsDNA-Binding ProteinsGene Expression RegulationGene Knockdown TechniquesHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsMiceNuclear ProteinsProtein-Tyrosine KinasesProto-Oncogene ProteinsSignal TransductionTransforming Growth Factor betaUbiquitin-Protein LigasesAutophagy-Related ProteinsDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsNuclear ProteinsProtein-Tyrosine KinasesProto-Oncogene ProteinsRB1CC1 protein, humanRb1cc1 protein, mouseRNF111 protein, humanRnf111 protein, mouseSKIL protein, humanSkil protein, mouseSKI protein, humanTransforming Growth Factor betaUbiquitin-Protein Ligases

Identifiers

PMID21795712
PMCPMC3173165
OpenAlexW1981006870

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.