Evidence map›Paper›PMID 7581520›Full record

ArticleTransgenic research1995

An in vivo analysis of transcriptional elements in the mouse alpha-myosin heavy chain gene promoter.

H Rindt, A Subramaniam, J Robbins

Abstract read
PubMed Publisher
In one paragraph

Article in Transgenic research, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-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

15 citing papers in PubMed, 40 citations in OpenAlex.

  1. ExcessiveCirculation · 2021
    Article
  2. Network-based predictions of in vivo cardiac hypertrophy.Journal of molecular and cellular cardiology · 2018
    Article
  3. Article
  4. Giving credence to controls: Avoiding the false phenotype.Journal of molecular and cellular cardiology · 2015
    Article
  5. Article
  6. Normal cardiac function in mice with supraphysiological cardiac creatine levels.American journal of physiology. Heart and circulatory physiology · 2014
    Article
  7. Article
  8. Article
  9. Article
  10. Mice with cardiomyocyte-specific disruption of the endothelin-1 gene are resistant to hyperthyroid cardiac hypertrophy.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

3 authors at 1 institution in 1 country.

H RindtDepartment of Pediatrics, Children's Hospital Research Foundation, Cincinnati, OH 45229-3039, USA.
A Subramaniam
J Robbins
Cincinnati Children's Hospital Medical Center · US

Funding

TRANSCRIPTIONAL CONTROL OF CARDIAC MYOSINSP01HL022619 · NHLBI · UNIVERSITY OF CINCINNATI · PI SCHWARTZ, ARNOLD · 1985 to 2003
$6.1M
SPATIAL RELATIONSHIPS IN CARDIAC TROPONIN--ACIDOSIS AND PHOSPHORYLATIONP01HL041496 · NHLBI · UNIVERSITY OF CINCINNATI · PI ROBBINS, JEFFREY · 1988 to 2000
$2.6M
CARDIOGENESIS DURING DIFFERENTIATION AND DEVELOPMENTP01HL046826 · NHLBI · UNIVERSITY OF CINCINNATI · PI ROBBINS, JEFFREY · 1991 to 1995
–
NHLBI NIH HHS HL22619NHLBI NIH HHS HL41496NHLBI NIH HHS HL46826
6 · The paper itself

Abstract

During development in the murine ventricle, there is a switch in myosin heavy chain gene (MyHC) transcription. The beta-MyHC is expressed in the ventricles during foetal development, but is shut down at or around birth, at which time alpha-MyHC transcription is activated. This antithetical switch is thought to be mediated by circulating levels of thyroid hormone (TH) and both low and high affinity thyroid response elements (TREs) have been identified in the proximal promoter region of the murine alpha-MyHC. Myosin gene expression in the atria is relatively unaffected by the TH status. Previously, we used site-directed mutagenesis of the promoter in a transgenic analysis to define those elements responsible for high levels of transcription in vivo. These analyses focused on the role(s) of two cis elements, TRE1 and TRE2 that are located at -129 to -149 and -102 to -120, respectively, on the alpha-MyHC promoter. Although the elements' ablation had differential effects on transgene expression, neither single mutation abolished transgene expression completely. Here, we show that mutating both elements results in a complete inactivation of the transgene in both ventricles and atria under euthyroid conditions. However, expression still can be detected in the hyperthyroid state, implying that, although the TRE1 and TRE2 elements are critical elements for high levels of alpha-MyHC transcription in vivo, other promoter sites can mediate at least some degree of transcriptional activation.

Indexed as

Atrial FunctionVentricular FunctionAnimalsBase SequenceChloramphenicol O-AcetyltransferaseGene Expression Regulation, DevelopmentalHyperthyroidismMiceMice, TransgenicMolecular Sequence DataMutationMyosin Heavy ChainsPromoter Regions, GeneticRecombinant Fusion ProteinsThyroid GlandThyroxineChloramphenicol O-AcetyltransferaseMyosin Heavy ChainsRecombinant Fusion ProteinsThyroxine

Identifiers

PMID7581520
OpenAlexW2082287297

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.