Evidence map›Paper›PMID 20610769›Full record

ArticleAmerican journal of physiology. Cell physiology2010

Abl activation regulates the dissociation of CAS from cytoskeletal vimentin by modulating CAS phosphorylation in smooth muscle.

Li Jia, Dale D Tang

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. GRespiratory research · 2024
    Review
  2. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  3. Article
  4. Reorganization of the Vimentin Network in Smooth Muscle.Journal of engineering and science in medical diagnostics and therapy · 2019
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. c-Abl tyrosine kinase regulates cytokinesis of human airway smooth muscle cells.American journal of respiratory cell and molecular biology · 2014
    Article
  15. Article
  16. Role of c-Abl tyrosine kinase in smooth muscle cell migration.American journal of physiology. Cell physiology · 2014
    Article
  17. Airway smooth muscle in airway reactivity and remodeling: what have we learned?American journal of physiology. Lung cellular and molecular physiology · 2013
    Review
  18. Article
  19. Article
  20. Raf-1, actin dynamics, and abelson tyrosine kinase in human airway smooth muscle cells.American journal of respiratory cell and molecular biology · 2013
    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

2 authors at 1 institution in 1 country.

Li JiaCenter for Cardiovascular Sciences, Albany Medical College, Albany, New York, USA.
Dale D Tang
Albany Medical Center Hospital · US

Funding

Reorganization of the Actin Cytoskeleton in Airway Smooth MuscleR01HL110951 · NHLBI · ALBANY MEDICAL COLLEGE · PI TANG, DALE D. · 2012 to 2022
$3.6M
Cytoskeletal Regulation of Airway Smooth MuscleR01HL113208 · NHLBI · ALBANY MEDICAL COLLEGE · PI TANG, DALE D. · 2012 to 2016
$1.7M
NHLBI NIH HHS R01 HL110951NHLBI NIH HHS R01 HL113208
6 · The paper itself

Abstract

Abl is a nonreceptor tyrosine kinase that is required for smooth muscle contraction. However, the mechanism by which Abl regulates smooth muscle contraction is not completely understood. In the present study, Abl underwent phosphorylation at Tyr412 (an index of Abl activation) in smooth muscle in response to contractile activation. Treatment with a cell-permeable decoy peptide, but not the control peptide, attenuated Abl phosphorylation during contractile stimulation. Treatment with the decoy peptide did not affect the association of Abl with the cytoskeletal protein vinculin and the spatial location of vinculin in smooth muscle. Inhibition of Abl phosphorylation by the decoy peptide attenuated the agonist-induced phosphorylation of Crk-associated substrate (CAS), an adapter protein participating in the signaling processes that regulate force development in smooth muscle. Additionally, previous studies have shown that contractile stimulation triggers the dissociation of CAS from the vimentin network, which is important for cytoskeletal signaling and contraction in smooth muscle. In this report, the decrease in the amount of CAS in cytoskeletal vimentin in response to contractile activation was reversed by the Abl inhibition with the decoy peptide. Moreover, force development and the enhancement of F-actin-to-G-actin ratios (an indication of actin polymerization) upon contractile activation were also attenuated by the Abl inhibition. However, myosin phosphorylation induced by contractile activation was not affected by the inhibition of Abl. These results suggest that Abl regulates the dissociation of CAS from the vimentin network, actin polymerization, and contraction by modulating CAS phosphorylation in smooth muscle.

Indexed as

AnimalsCarotid ArteriesCrk-Associated Substrate ProteinEnzyme ActivationIn Vitro TechniquesMaleMyocytes, Smooth MusclePhosphorylationProto-Oncogene Proteins c-ablRatsRats, Sprague-DawleyVimentinBcar1 protein, ratCrk-Associated Substrate ProteinProto-Oncogene Proteins c-ablVimentin

Identifiers

PMID20610769
PMCPMC3774473
OpenAlexW1989371993

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.