Evidence map›Paper›PMID 8657140›Full record

ArticleMolecular and cellular biology1996

Analysis of muscle creatine kinase gene regulatory elements in skeletal and cardiac muscles of transgenic mice.

D B Donoviel, M A Shield, J N Buskin, H S Haugen, C H Clegg, S D Hauschka

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Article
  3. Targeted epigenetic repression by CRISPR/dSaCas9 suppresses pathogenicMolecular therapy. Methods & clinical development · 2021
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Nuclear function of Smad7 promotes myogenesis.Molecular and cellular biology · 2010
    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 2 institutions in 3 countries.

D B DonovielDepartment of Biochemistry, University of Washington, Seattle, 98195-7350, USA.
M A Shield
J N Buskin
H S Haugen
C H Clegg
S D Hauschka
University of Washington · USBristol-Myers Squibb (Germany) · DE

Funding

Vasular cell origins and fates in granulation tissueP01HL003174 · NHLBI · UNIVERSITY OF WASHINGTON · PI SCHWARTZ, EMILY J. · 1985 to 2007
$13.8M
Striated Muscle Gene Transcription and Regulatory Gene Cassettes for Gene TherapyR01AR018860 · NIAMS · UNIVERSITY OF WASHINGTON · PI HAUSCHKA, STEPHEN DENISON · 1986 to 2012
$3.4M
REGULATION OF SKELETAL MUSCLE DIFFERENTIATIONR37AR018860 · NIAMS · UNIVERSITY OF WASHINGTON · PI HAUSCHKA, STEPHEN DENISON · 1993 to 2002
$1.0M
HEART-SPECIFIC CREATINE KINASE REGULATORY ELEMENTSR01HL039070 · NHLBI · UNIVERSITY OF WASHINGTON · PI HAUSCHKA, STEPHEN DENISON · 1987 to 1992
–
NHLBI NIH HHS HL39070NHLBI NIH HHS P01-HL03174NIAMS NIH HHS AR18860
6 · The paper itself

Abstract

Regulatory regions of the mouse muscle creatine kinase (MCK) gene, previously discovered by analysis in cultured muscle cells, were analyzed in transgenic mice. The 206-bp MCK enhancer at nt-1256 was required for high-level expression of MCK-chloramphenicol acetyltransferase fusion genes in skeletal and cardiac muscle; however, unlike its behavior in cell culture, inclusion of the 1-kb region of DNA between the enhancer and the basal promoter produced a 100-fold increase in skeletal muscle activity. Analysis of enhancer control elements also indicated major differences between their properties in transgenic muscles and in cultured muscle cells. Transgenes in which the enhancer right E box or CArG element were mutated exhibited expression levels that were indistinguishable from the wild-type transgene. Mutation of three conserved E boxes in the MCK 1,256-bp 5' region also had no effect on transgene expression in thigh skeletal muscle expression. All these mutations significantly reduced activity in cultured skeletal myocytes. However, the enhancer AT-rich element at nt - 1195 was critical for expression in transgenic skeletal muscle. Mutation of this site reduced skeletal muscle expression to the same level as transgenes lacking the 206-bp enhancer, although mutation of the AT-rich site did not affect cardiac muscle expression. These results demonstrate clear differences between the activity of MCK regulatory regions in cultured muscles cells and in whole adult transgenic muscle. This suggests that there are alternative mechanism of regulating the MCK gene in skeletal and cardiac muscle under different physiological states.

Indexed as

Regulatory Sequences, Nucleic AcidAnimalsBase SequenceCells, CulturedChloramphenicol O-AcetyltransferaseCreatine KinaseEnhancer Elements, GeneticMiceMice, TransgenicMolecular Sequence DataMuscle, SkeletalMyocardiumOrgan SpecificityPromoter Regions, GeneticRecombinant Fusion ProteinsChloramphenicol O-AcetyltransferaseCreatine KinaseRecombinant Fusion Proteins

Identifiers

PMID8657140
PMCPMC231151
OpenAlexW2108922768

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.