Evidence map›Paper›PMID 10620510›Full record

ArticleThe Biochemical journal2000

The winged-helix/forkhead protein myocyte nuclear factor beta (MNF-beta) forms a co-repressor complex with mammalian sin3B.

Q Yang, Y Kong, B Rothermel, D J Garry, R Bassel-Duby, R S Williams

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

37 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Zebrafish sin3b mutants are viable but have size, skeletal, and locomotor defects.Developmental dynamics : an official publication of the American Association of Anatomists · 2017
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Sin3 interacts with Foxk1 and regulates myogenic progenitors.Molecular and cellular biochemistry · 2012
    Article
  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

6 authors at 1 institution in 1 country.

Q YangDepartment of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., NB11.200, Dallas, TX 75390-8573, USA.
Y Kong
B Rothermel
D J Garry
R Bassel-Duby
R S Williams
The University of Texas Southwestern Medical Center · US

Funding

Transcriptional control of muscle growth and remodelingP01HL006296 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N · 1985 to 2006
$14.8M
TRAINING IN CARDIOVASCULAR RESEARCHT32HL007360 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 1985 to 2012
$11.8M
WINGED HELIX TRANSCRIPTION FACTORS AND MYOGENESISK08HL003231 · NHLBI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI GARRY, DANIEL J. · 1995 to 2001
$224k
NHLBI NIH HHS HL03231NHLBI NIH HHS HL06296NHLBI NIH HHS HL07360
6 · The paper itself

Abstract

Winged-helix/forkhead proteins regulate developmental events in both invertebrate and vertebrate organisms, but biochemical functions that establish a mechanism of action have been defined for only a few members of this extensive gene family. Here we demonstrate that MNF (myocyte nuclear factor)-beta, a winged-helix protein expressed selectively and transiently in myogenic precursor cells of the heart and skeletal muscles, collaborates with proteins of the mammalian Sin3 (mSin3) family to repress transcription. Mutated forms of MNF-beta that fail to bind mSin3 are defective in transcriptional repression and in negative growth regulation, an overexpression phenotype revealed in oncogenic transformation assays. These data extend the known repertoire of transcription factors with which mSin3 proteins can function as co-repressors to include members of the winged-helix gene family. Transcriptional repression by MNF-beta-mSin3 complexes may contribute to the co-ordination of cellular proliferation and terminal differentiation of myogenic precursor cells.

Indexed as

Helix-Loop-Helix MotifsAdenovirus E1A ProteinsAnimalsBinding SitesCell DifferentiationCell Transformation, NeoplasticDNA-Binding ProteinsForkhead Transcription FactorsGenes, Tumor SuppressorMiceMolecular Sequence DataMusclesMuscle, SkeletalMyocardiumNuclear ProteinsPeptide FragmentsAdenovirus E1A ProteinsDNA-Binding ProteinsForkhead Transcription FactorsFoxk1 protein, mouseNuclear ProteinsPeptide FragmentsProtein IsoformsProto-Oncogene Proteins c-mycras ProteinsRecombinant ProteinsRepressor ProteinsSin3b protein, mouseTranscription Factors

Identifiers

PMID10620510
PMCPMC1220762
OpenAlexW1993475336

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.