scholarly journals Posttranslational Modifications of Myosin Light Chains Determine the Protein Fate

10.5772/28656 ◽  
2012 ◽  
Author(s):  
Virgilio J. J. Cadete ◽  
Grzegorz Sawicki
Keyword(s):  
Posttranslational Modifications ◽  
Light Chains ◽  
Myosin Light Chains

The expression of myosin light chains and tropomyosin in human muscle biopsies with histochemical type 1 and type 2 fiber deficiency

1990 ◽  
Vol 13 (3) ◽  
pp. 209-214 ◽  
Author(s):  
Carol S. Giometti ◽  
Moris J. Danon
Keyword(s):  
Human Muscle ◽  
Light Chains ◽  
Myosin Light Chains ◽  
Muscle Biopsies

scholarly journals Resolution of Myocardial Myosin Light Chains by Two-Dimensional Gel Electrophoresis

1974 ◽  
Vol 249 (3) ◽  
pp. 994-996
Author(s):  
John McPherson ◽  
Robert R. Traut ◽  
Dean T. Mason ◽  
Robert Zelis ◽  
Joan Wikman-Coffelt
Keyword(s):  
Gel Electrophoresis ◽  
Light Chains ◽  
Myosin Light Chains ◽  
Two Dimensional ◽  
Two Dimensional Gel Electrophoresis

Changes in the composition of cardiac muscle myosin light chains during cardiac diseases

BIOPHYSICS ◽  
2012 ◽  
Vol 57 (2) ◽  
pp. 201-214
Author(s):  
Z. A. Podlubnaya ◽  
Ya. N. Khalina ◽  
D. A. Bledjyanz
Keyword(s):  
Cardiac Muscle ◽  
Light Chains ◽  
Myosin Light Chains ◽  
Cardiac Diseases ◽  
Muscle Myosin

α-Actinin and myosin light chains in congenital nemaline myopathy

1990 ◽  
Vol 6 (3) ◽  
pp. 171-174 ◽  
Author(s):  
Carina Wallgren-Pettersson ◽  
Pirkko Arjomaa ◽  
Christer Holmberg
Keyword(s):  
Nemaline Myopathy ◽  
Light Chains ◽  
Myosin Light Chains

scholarly journals The atypical structure and function of newborn arterial endothelium is mediated by Rho/Rho kinase signaling

2014 ◽  
Vol 307 (4) ◽  
pp. H628-H632 ◽  
Author(s):  
Sheila Flavahan ◽  
Nicholas A. Flavahan
Keyword(s):  
Laser Scanning ◽  
Rho Kinase ◽  
Laser Scanning Microscopy ◽  
Scanning Microscopy ◽  
Stress Fibers ◽  
Light Chains ◽  
Myosin Light Chains ◽  
Kinase Signaling ◽  
No Donor ◽  
Kinase Inhibition

Endothelium of fetal or newborn arteries is atypical, displaying actin stress fibers and reduced nitric oxide (NO)-mediated dilatation. This study tested the hypothesis that Rho/Rho kinase signaling, which promotes endothelial stress fibers and inhibits endothelial dilatation, contributed to this phenotype. Carotid arteries were isolated from newborn [ postnatal day 1 (P1)], P7, and P21 mice. Endothelial dilatation to acetylcholine (pressure myograph) was minimal at P1, increased at P7, and further increased at P21. Inhibition of Rho (C3 transferase) or Rho kinase (Y27632, fasudil) significantly increased dilatation to acetylcholine in P1 arteries but had no effect in P7 or P21 arteries. After inhibition of NO synthase ( NG-nitro-l-arginine methyl ester), Rho kinase inhibition no longer increased acetylcholine responses in P1 arteries. Rho kinase inhibition did not affect dilatation to the NO donor DEA-NONOate. The endothelial actin cytoskeleton was labeled with phalloidin and visualized by laser-scanning microscopy. In P1 arteries, the endothelium had prominent transcytoplasmic stress fibers, whereas in P7 and P21 arteries, the actin fibers had a significantly reduced intensity and were restricted to cell borders. Phosphorylation of myosin light chains, a Rho kinase substrate, was highest in P1 endothelium and significantly reduced in P7 and P21 endothelium (laser-scanning microscopy). In P1 arteries, inhibition of Rho (C3 transferase) or Rho kinase (Y27632) significantly reduced the intensity of actin fibers, which were restricted to cell borders. Similarly, in P1 arteries, Rho inhibition significantly reduced endothelial levels of phosphorylated myosin light chains. These results indicate that the atypical function and morphology of newborn endothelium is mediated by Rho/Rho kinase signaling.

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