Evidence map›Paper›PMID 10517807›Full record

ArticleThe Journal of physiology1999

Reconstitution of protein kinase C-induced contractile Ca2+ sensitization in triton X-100-demembranated rabbit arterial smooth muscle.

T Kitazawa, N Takizawa, M Ikebe, M Eto

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 151 citations in OpenAlex.

  1. Review
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  7. Review
  8. MYPT1 isoforms expressed in HEK293T cells are differentially phosphorylated after GTPγS treatment.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2016
    Article
  9. Review
  10. Vascular O-GlcNAcylation augments reactivity to constrictor stimuli by prolonging phosphorylated levels of the myosin light chain.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Article
  11. Article
  12. Smooth muscle-selective CPI-17 expression increases vascular smooth muscle contraction and blood pressure.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  13. Article
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  17. Role for PKCβ in enhanced endothelin-1-induced pulmonary vasoconstrictor reactivity following intermittent hypoxia.American journal of physiology. Lung cellular and molecular physiology · 2011
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

T KitazawaDepartment of Physiology and Biophysics, Georgetown University Medical Center, Washington, DC 20007, USA. tkitaz01@gusun.georgetown.edu
N Takizawa
M Ikebe
M Eto
University of Massachusetts Chan Medical School · USGeorgetown University Medical Center · USUniversity of Virginia · US

Funding

PROTEIN KINASES ON SMOOTH MUSCLE REGULATIONR01HL061426 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI IKEBE, MITSUO · 1999 to 2002
$1.3M
G PROTEIN-MEDIATED CA++ SENSITIZATION IN SMOOTH MUSCLER01HL051824 · NHLBI · GEORGETOWN UNIVERSITY · PI KITAZAWA, TOSHIO · 1993 to 2002
$952k
FUNCTION OF RHO PATHWAY ON SMOOTH MUSCLE CONTRACTIONR01HL060831 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI IKEBE, MITSUO · 1998 to 2000
$329k
NHLBI NIH HHS HL51824NHLBI NIH HHS HL60831NHLBI NIH HHS HL61426
6 · The paper itself

Abstract

1. Triton X-100-demembranated smooth muscle loses Ca2+-sensitizing responsiveness to protein kinase C (PKC) activators while intact and alpha-toxin-permeabilized smooth muscles remain responsive. We attempted to reconstitute the contractile Ca2+ sensitization by PKC in the demembranated preparations. 2. Western blot analyses showed that the content of the PKC alpha-isoform (PKCalpha) was markedly reduced and that the smooth muscle-specific protein phosphatase-1 inhibitor protein CPI-17 was not detectable, while the amount of calponin and actin still remained similar to those of intact strips. 3. Unphosphorylated recombinant CPI-17 alone induced a small but significant contraction at constant Ca2+. Isoform-selective PKC inhibitors inhibited unphosphorylated but not pre-thiophosphorylated CPI-17-induced contraction, suggesting that in situ conventional PKC isoform(s) can phosphorylate CPI-17. 4. Exogenously replenishing PKCalpha alone did not induce potentiation of contraction and only slowly increased myosin light chain (MLC) phosphorylation at submaximal Ca2+. 5. PKC in the presence of CPI-17, but not the [T38A]-CPI mutant, markedly induced potentiation of both contraction and MLC phosphorylation. CPI-17 itself was phosphorylated. 6. In in vitro experiments, CPI-17 was a much better substrate for PKCalpha than calponin, caldesmon, MLC and myosin. 7. Our results indicate that PKC requires CPI-17 phosphorylation at Thr-38 but not calponin for reconstitution of the contractile Ca2+ sensitization in the demembranated arterial smooth muscle.

Indexed as

AnimalsBlotting, WesternCalciumCell MembraneEnzyme ActivatorsIn Vitro TechniquesIsoenzymesMaleMuscle ContractionMuscle, Smooth, VascularOctoxynolPhorbol 12,13-DibutyratePhosphorylationProtein Kinase CRabbitsRecombinant ProteinsCalciumEnzyme ActivatorsIsoenzymesOctoxynolPhorbol 12,13-DibutyrateProtein Kinase CRecombinant Proteins

Identifiers

PMID10517807
PMCPMC2269567
OpenAlexW2068483215

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.