التفاصيل البيبلوغرافية
| العنوان: |
A role for the tyrosine kinase Pyk2 in depolarization‐induced contraction of vascular smooth muscle (609.3) |
| المؤلفون: |
Mills, Ryan, Mita, Mitsuo, Sutherland, Cindy, Walsh, Michael |
| المصدر: |
The FASEB Journal ; volume 28, issue S1 ; ISSN 0892-6638 1530-6860 |
| بيانات النشر: |
Wiley |
| سنة النشر: |
2014 |
| المجموعة: |
Wiley Online Library (Open Access Articles via Crossref) |
| الوصف: |
Background: Depolarization of vascular smooth muscle induces rapid (phasic) contraction followed by sustained (tonic) contraction. The latter is due to activation of the RhoA/Rho‐kinase pathway via genistein‐sensitive tyrosine phosphorylation. Objective: To determine if the Ca2 + ‐dependent tyrosine kinase Pyk2 is involved in depolarization‐induced sustained contraction. Methods: Depolarization of endothelium‐free rat caudal arterial smooth muscle was induced by high extracellular [K + ] in the absence or presence of Pyk2 inhibitors. Isometric force was measured with a force transducer and Pyk2 activation (autophosphorylation of Y402) was quantified by western blotting with phosphospecific antibodies. Results: Depolarization induced Pyk2‐Y402 phosphorylation in a time‐dependent manner. Pyk2 inhibitors (sodium salicylate, PF431396 and others) prevented Y402 phosphorylation and inhibited K+‐induced contraction. Vanadate (tyrosine phosphatase inhibitor)‐, but not calyculin A (Ser/Thr phosphatase inhibitor)‐induced contraction was also inhibited by Pyk2 inhibition. Conclusion: Membrane depolarization induces phosphorylation and activation of Pyk2, which is required for the tonic phase of K+‐induced contraction. |
| نوع الوثيقة: |
article in journal/newspaper |
| اللغة: |
English |
| DOI: |
10.1096/fasebj.28.1_supplement.609.3 |
| الإتاحة: |
https://doi.org/10.1096/fasebj.28.1_supplement.609.3Test |
| حقوق: |
http://onlinelibrary.wiley.com/termsAndConditions#vorTest |
| رقم الانضمام: |
edsbas.AA47F558 |
| قاعدة البيانات: |
BASE |
