Evidence map›Paper›PMID 19429828›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

Nonmuscle myosin is regulated during smooth muscle contraction.

Samantha L Yuen, Ozgur Ogut, Frank V Brozovich

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Structural basis of nonmuscle myosin-2 autoinhibition mechanisms.bioRxiv : the preprint server for biology · 2025
    Article
  3. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. TheMolecular biology of the cell · 2020
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

Samantha L YuenCardiovascular Diseases, Mayo Medical School, Rochester, MN 55905, USA.
Ozgur Ogut
Frank V Brozovich
Mayo Clinic · US

Funding

REGULATION OF SMOOTH MUSCLE CONTRACTILE PROPERTIESR01HL064137 · NHLBI · MAYO CLINIC ROCHESTER · PI BROZOVICH, FRANK V · 2000 to 2008
$2.5M
REGULATION OF VASCULAR SMOOTH MUSCLE CONTRACTIONR01HL044181 · NHLBI · MAYO CLINIC · PI BROZOVICH, FRANK V · 1997 to 2005
$2.0M
Regulation of Contractility During Ischemia-ReperfusionR01HL078845 · NHLBI · MAYO CLINIC ROCHESTER · PI OGUT, OZGUR · 2006 to 2010
$1.7M
Vascular Reactivity in Heart FailureR01HL069894 · NHLBI · MAYO CLINIC ROCHESTER · PI BROZOVICH, FRANK V · 2003 to 2006
$1.5M
REGULATION OF VASCULAR SMOOTH MUSCLE CONTRACTIONR29HL044181 · NHLBI · GRADUATE HOSPITAL (PHILADELPHIA) · PI BROZOVICH, FRANK V · 1990 to 1994
–
NHLBI NIH HHS HL44181NHLBI NIH HHS HL64137NHLBI NIH HHS HL69894NHLBI NIH HHS HL78845
6 · The paper itself

Abstract

The participation of nonmuscle myosin in force maintenance is controversial. Furthermore, its regulation is difficult to examine in a cellular context, as the light chains of smooth muscle and nonmuscle myosin comigrate under native and denaturing electrophoresis techniques. Therefore, the regulatory light chains of smooth muscle myosin (SM-RLC) and nonmuscle myosin (NM-RLC) were purified, and these proteins were resolved by isoelectric focusing. Using this method, intact mouse aortic smooth muscle homogenates demonstrated four distinct RLC isoelectric variants. These spots were identified as phosphorylated NM-RLC (most acidic), nonphosphorylated NM-RLC, phosphorylated SM-RLC, and nonphosphorylated SM-RLC (most basic). During smooth muscle activation, NM-RLC phosphorylation increased. During depolarization, the increase in NM-RLC phosphorylation was unaffected by inhibition of either Rho kinase or PKC. However, inhibition of Rho kinase blocked the angiotensin II-induced increase in NM-RLC phosphorylation. Additionally, force for angiotensin II stimulation of aortic smooth muscle from heterozygous nonmuscle myosin IIB knockout mice was significantly less than that of wild-type littermates, suggesting that, in smooth muscle, activation of nonmuscle myosin is important for force maintenance. The data also demonstrate that, in smooth muscle, the activation of nonmuscle myosin is regulated by Ca(2+)-calmodulin-activated myosin light chain kinase during depolarization and a Rho kinase-dependent pathway during agonist stimulation.

Indexed as

Amino Acid SequenceAngiotensin IIAnimalsBlotting, WesternChickensElectrophoresis, Gel, Two-DimensionalGene Expression RegulationMass SpectrometryMiceMice, TransgenicMuscle ContractionMuscle, SmoothMyosin Light ChainsMyosinsNonmuscle Myosin Type IIBPhosphorylationAngiotensin IIMyosin Light ChainsMyosinsNonmuscle Myosin Type IIBRecombinant Proteinsrho-Associated Kinases

Identifiers

PMID19429828
PMCPMC2711724
OpenAlexW2069129735

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.