Evidence map›Paper›PMID 1922033›Full record

ArticleMolecular and cellular biology1991

Activation of skeletal alpha-actin gene transcription: the cooperative formation of serum response factor-binding complexes over positive cis-acting promoter serum response elements displaces a negative-acting nuclear factor enriched in replicating myoblasts and nonmyogenic cells.

T C Lee, K L Chow, P Fang, R J Schwartz

Abstract read
In one paragraph

Article in Molecular and cellular biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
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  5. The STARS signaling pathway: a key regulator of skeletal muscle function.Pflugers Archiv : European journal of physiology · 2014
    Review
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  14. Review
  15. Article
  16. Activation of the skeletal alpha-actin promoter during muscle regeneration.Journal of muscle research and cell motility · 1998
    Article
  17. Review
  18. Article
  19. Molecular cloning of a novel mouse gene with predominant muscle and neural expression.Mammalian genome : official journal of the International Mammalian Genome Society · 1998
    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

4 authors at 1 institution in 1 country.

T C LeeDepartment of Cell Biology, Baylor College of Medicine, Houston, Texas 77030.
K L Chow
P Fang
R J Schwartz
Baylor College of Medicine · US

Funding

DIFFERENTIATION OF ACTIN MYOGENESISR01HL038401 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI SCHWARTZ, ROBERT · 1987 to 1991
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NHLBI NIH HHS 87-HL-26-HNHLBI NIH HHS HL38401
6 · The paper itself

Abstract

Three upstream CBAR cis-acting promoter elements, containing the inner core CC(A/T)6GG of the serum response element (SRE), are required for myogenic cell type-restricted expression of the avian skeletal alpha-actin gene (K.L. Chow and R.J. Schwartz, Mol. Cell. Biol. 10:528-538, 1990). These actin SRE elements display differential binding properties with two distinct nuclear proteins, serum response factor (SRF) and another factor described here as F-ACT1. SRF is able to bind to all actin SREs with various affinities. This multisite interaction is marked by cooperative binding events in that the two high-affinity proximal and distal SREs facilitate the weak central-site interaction with SRF, leading to the formation of a higher-order SRF-promoter complex. Functional analyses reveal that undisrupted multiple SRF-DNA interactions are absolutely essential for promoter activity in myogenic cells. F-ACT1, present at higher levels in nonmyogenic cells and replicating myoblasts than in myotubes, binds solely to the proximal SRE, and its binding is mutually exclusive with that of SRF owing to their overlapping base contacts. The cooperative promoter binding by SRF, however, can effectively displace prebound F-ACT1. In addition, an intact F-ACT1 binding site acts as a negative promoter element by restricting developmentally timed expression in myoblasts. F-ACT1 may therefore act as a repressor of skeletal alpha-actin gene transcription. This interplay between F-ACT1 and SRF may constitute a developmental as well as a physiologically regulated mechanism which modulates sarcomeric actin gene expression.

Indexed as

ActinsAnimalsBase SequenceCells, CulturedChick EmbryoDNA-Binding ProteinsEscherichia coliGene Expression RegulationMolecular Sequence DataMusclesMutationNuclear ProteinsOligonucleotidesPromoter Regions, GeneticRepressor ProteinsSerum Response FactorActinsDNA-Binding ProteinsNuclear ProteinsOligonucleotidesRepressor ProteinsSerum Response Factor

Identifiers

PMID1922033
PMCPMC361518
OpenAlexW2301712053

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.