Evidence map›Paper›PMID 19403597›Full record

ArticleThe Journal of physiology2009

Activation by Ca2+/calmodulin of an exogenous myosin light chain kinase in mouse arteries.

H Raina, J Zacharia, M Li, W G Wier

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 27% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Regulation of myosin light-chain phosphorylation and its roles in cardiovascular physiology and pathophysiology.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Imaging sympathetic neurogenic CaAutonomic neuroscience : basic & clinical · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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.

H RainaDepartment of Physiology, School of Medicine, University of Maryland, Baltimore, MD 21201, USA.
J Zacharia
M Li
W G Wier
University of Maryland, Baltimore · US

Funding

Sympathetic Neurotransmitters and Ouabain HypertensionP01HL078870 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BLAUSTEIN, MORDECAI P · 2005 to 2009
$9.9M
Neurogenic Calcium Signals in Small ArteriesR01HL073094 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI WIER, WITHROW GIL · 2004 to 2007
$1.2M
NHLBI NIH HHS HL 073094NHLBI NIH HHS HL 078870NHLBI NIH HHS P01 HL078870NHLBI NIH HHS R01 HL073094
6 · The paper itself

Abstract

Activation of myosin light chain kinase (MLCK) and other kinases was studied in the arteries of transgenic mice that express an optical fluorescence resonance energy transfer (FRET) MLCK activity biosensor. Binding of Ca(2+)/calmodulin (Ca(2+)/CaM) induces an increase in MLCK activity and a change in FRET. After exposure to high external [K(+)], intracellular [Ca(2+)] (fura-2 ratio or fluo-4 fluorescence) and MLCK activity both increased rapidly to an initial peak and then declined, rapidly at first and then very slowly. After an initial peak ('phasic') force was constant or increased slowly (termed 'tonic' force). Inhibition of rho-kinase (Y-27632) decreased tonic force more than phasic, but had little effect on [Ca(2+)] and MLCK activation. Inhibition of PKCalpha and PKCbeta with Gö6976 had no effect. KN-93, an inhibitor of CaMK II, markedly reduced force, MLCK FRET and [Ca(2+)]. Applied during tonic force, forskolin caused a rapid decrease in MLCK FRET ratio and force, but no change in Ca(2+), suggesting a cAMP mediated decrease in affinity of MLCK for Ca(2+)/CaM. However, receptor (beta-adrenergic) activated increases in cAMP during KCl were ineffective in causing relaxation, changes in [Ca(2+)], or MLCK FRET. At the same tonic force, MLCK FRET ratio activated by alpha(1)-adrenoceptors was approximately 60% of that activated by KCl. In conclusion, MLCK activity of arterial smooth muscle during KCl-induced contraction is determined primarily by Ca(2+)/CaM. Rho-kinase is activated, by unknown mechanisms, and increases 'Ca(2+) sensitivity' significantly. Forskolin mediated increases in cAMP, but not receptor mediated increases in cAMP cause a rapid decrease in the affinity of MLCK for Ca(2+)/CaM.

Indexed as

VasoconstrictionAdenylyl CyclasesAnimalsBiosensing TechniquesCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2CalmodulinCyclic AMPCyclic AMP-Dependent Protein KinasesEnzyme ActivationEnzyme ActivatorsFluorescence Resonance Energy TransferKineticsMesenteric ArteriesMiceMice, TransgenicAdenylyl CyclasesCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2CalmodulinCyclic AMPCyclic AMP-Dependent Protein KinasesEnzyme ActivatorsMyosin-Light-Chain KinasePotassiumProtein Kinase CProtein Kinase InhibitorsReceptors, Adrenergic, beta-1rho-Associated KinasesVasoconstrictor Agents

Identifiers

PMID19403597
PMCPMC2714024
OpenAlexW1552222951

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.