The murine atrial myosin light chain-2 gene:a member of an evolutionarily conserved family of contractile proteins

2000 ◽  
Vol 90 (3-4) ◽  
pp. 248-252 ◽  
Author(s):  
P.A. Doevendans ◽  
R. Bronsaer ◽  
P.R. Lozano ◽  
S. Kubalak ◽  
M. van Bilsen
Keyword(s):  
Light Chain ◽  
Myosin Light Chain ◽  
Contractile Proteins ◽  
Myosin Light Chain 2 ◽  
Evolutionarily Conserved ◽  
Atrial Myosin

scholarly journals Chamber specification of atrial myosin light chain-2 expression precedes septation during murine cardiogenesis

1994 ◽  
Vol 269 (24) ◽  
pp. 16961-16970
Author(s):  
S.W. Kubalak ◽  
W.C. Miller-Hance ◽  
T.X. O'Brien ◽  
E. Dyson ◽  
K.R. Chien
Keyword(s):  
Light Chain ◽  
Myosin Light Chain ◽  
Myosin Light Chain 2 ◽  
Atrial Myosin

scholarly journals Effects of Total Replacement of Atrial Myosin Light Chain-2 With the Ventricular Isoform in Atrial Myocytes of Transgenic Mice

Circulation ◽  
1998 ◽  
Vol 97 (15) ◽  
pp. 1508-1513 ◽  
Author(s):  
Corinn M. Pawloski-Dahm ◽  
Guojie Song ◽  
Darryl L. Kirkpatrick ◽  
Joe Palermo ◽  
James Gulick ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Atrial Myocytes ◽  
Total Replacement ◽  
Myosin Light Chain 2 ◽  
Atrial Myosin

Abstract WMP39: Protein Phosphatase 1 Regulatory Subunit 12C Contributes to Atrial Myosin Light Chain Dephosphorylation in Atrial Fibrillation

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Srikanth Perike ◽  
Katherina M Alsina ◽  
Arvind Sridhar ◽  
Dawood Darbar ◽  
Xander Wehrens ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Light Chain ◽  
Protein Phosphatase ◽  
Myosin Light Chain ◽  
Stroke Risk ◽  
Contractile Function ◽  
Protein Phosphatase 1 ◽  
Regulatory Subunit ◽  
Western Blots ◽  
Atrial Myosin

Background: Atrial fibrillation (AF) increases stroke risk five-fold. Atrial hypocontractility from atrial myosin light chain (MLC2a) dephosphorylation contributes to stroke risk in AF. Recent proteomic data has shown increased protein phosphatase 1 subunit 12C (PPP1R12C) targeting to MLC2a in AF. However, it is unclear whether PPP1R12C causes MLC2a dephosphorylation in AF. Objective: Determine whether increased PPP1R12C expression causes MLC2a dephosphorylation and increases AF risk. Methods: Western blots and co-IPs were performed to evaluate the relationship among PPP1R12C, PP1c and MLC2a in human atrial tissues (AF vs SR). Mice with either a knockout (KO) or lentiviral (LV) cardiac overexpression of PPP1R12C were evaluated with invasive EP studies for AF inducibility vs WT controls. Results: In human AF, PPP1R12C was increased 4-fold ( P <0.005, n=6) with an 88% reduction in S-19-MLC2a phosphorylation ( P <0.05, n=4). PPP1R12C-PP1c and PPP1R12C-MLC2a binding was increased 2-fold in AF ( P <0.05, n=6). AF burden in LV-12C mice increased nearly tenfold vs. KO and WT mice ( P <0.05, n=6). Conclusion: In human AF, increased PPP1R12C expression is associated with reduced P-MLC2a through enhanced binding with the PP1c catalytic subunit. This dephosphorylation is a likely contributor to atrial hypocontractility and stroke risk in AF. Additionally, increased PPP1R12C expression in mice increases AF risk. Future studies will examine the effects of increased PPP1R12C expression upon atrial contractile function in mice.

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