Smoothelin-like 1 deletion enhances myogenic reactivity of mesenteric arteries with alterations in PKC and myosin phosphatase signaling
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Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-018-36564-0.pdf
Reference42 articles.
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2. Borman, M. A., Freed, T. A., Haystead, T. A. & MacDonald, J. A. The role of the calponin homology domain of smoothelin-like 1 (SMTNL1) in myosin phosphatase inhibition and smooth muscle contraction. Mol Cell Biochem 327, 93–100, https://doi.org/10.1007/s11010-009-0047-z (2009).
3. van Eys, G. J., Niessen, P. M. & Rensen, S. S. Smoothelin in vascular smooth muscle cells. Trends Cardiovasc Med 17, 26–30, https://doi.org/10.1016/j.tcm.2006.11.001 (2007).
4. Murali, M. & MacDonald, J. A. Smoothelins and the Control of Muscle Contractility. Adv Pharmacol 81, 39–78, https://doi.org/10.1016/bs.apha.2017.10.001 (2018).
5. Wooldridge, A. A. et al. Deletion of the protein kinase A/protein kinase G target SMTNL1 promotes an exercise-adapted phenotype in vascular smooth muscle. J Biol Chem 283, 11850–11859, https://doi.org/10.1074/jbc.M708628200 (2008).
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