Evidence map›Paper›PMID 14530442›Full record

ArticleNucleic acids research2003

Sox6 regulation of cardiac myocyte development.

Orit Cohen-Barak, Zanhua Yi, Nobuko Hagiwara, Koshiro Monzen, Issei Komuro, Murray H Brilliant

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 30% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Differential expression of members of SOX family of transcription factors in failing human hearts.Translational research : the journal of laboratory and clinical medicine · 2022
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. SOX on tumors, a comfort or a constraint?Cell death discovery · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. SOX6 Downregulation InducesBioMed research international · 2017
    Article
  16. Article
  17. Review
  18. SOX6 and PDCD4 enhance cardiomyocyte apoptosis through LPS-induced miR-499 inhibition.Apoptosis : an international journal on programmed cell death · 2016
    Article
  19. 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

6 authors at 1 institution in 1 country.

Orit Cohen-BarakDepartment of Pediatrics, The University of Arizona College of Medicine, Steele Memorial Children's Research Center 1501 N. Campbell Avenue, Tucson, AZ 85724, USA.
Zanhua Yi
Nobuko Hagiwara
Koshiro Monzen
Issei Komuro
Murray H Brilliant
University of Arizona · US

Funding

GENETIC AND MOLECULAR ANALYSES OF MUTATIONSR01GM043840 · NIGMS · UNIVERSITY OF ARIZONA · PI BRILLIANT, MURRAY H · 1989 to 2002
$1.6M
NIGMS NIH HHS GM43840
6 · The paper itself

Abstract

A mouse mutation (p100H/p100H) has been identified that is associated with cardioskeletal myopathy, heart block, delayed growth and early postnatal death. The gene that is disrupted in this mutation encodes the transcription factor Sox6. P19CL6 cells were used as an in vitro cardiomyocyte differentiation system and revealed that Sox6 is expressed exclusively when the cells are committed to differentiate to beating cardiac myocytes. We used the yeast two-hybrid system to identify the Prtb (Proline-rich transcript of the brain) protein as a Sox6 interactor, and subsequently confirmed the interaction by co-immunoprecipitation. Prtb expression in P19CL6 cells increased with differentiation to beating cardiomyocytes. Using the P19CL6 cells stably transfected with noggin, an antagonist of BMP (Bone Morphogenic Protein), we found that BMP expression is required for Sox6 expression in cardiomyocyte differentiation. Surprisingly, the expression of the alpha1c-subunit gene of the L-type Ca2+ channel decreased in P19CL6 cells as they differentiated to beating cardiac cells. Ectopic expression of Sox6 or Prtb alone in P19CL6 cells caused down-regulation of L-type Ca2+ alpha1c expression, but when Sox6 and Prtb were co-transfected to the cells, L-type Ca2+ alpha1c remained at basal levels. A similar relationship of Sox6 and L-type Ca2+ alpha1c expression was seen in vivo (comparing wild-type and p(100H)/p(100H) mutant mice). Thus, Sox6 is within the BMP pathway in cardiac differentiation, interacts with Prtb and may play a critical role in the regulation of a cardiac L-type Ca2+ channel.

Indexed as

Transcription FactorsAnimalsBlotting, NorthernCalcium Channels, L-TypeCell DifferentiationCell Line, TumorDNA-Binding ProteinsFemaleGene ExpressionGenotypeHigh Mobility Group ProteinsHumansMaleMiceMice, Mutant StrainsMutationCalcium Channels, L-TypeDNA-Binding ProteinsHigh Mobility Group ProteinsL-type calcium channel alpha(1C)Peptidesprtb peptideRNA, MessengerSOX6 protein, humanSox6 protein, mouseSOXD Transcription FactorsTranscription Factors

Identifiers

PMID14530442
PMCPMC219484
OpenAlexW2078782153

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.