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Physical stimulation of cells in monolayer enhances gap junction function [ 23, 49, 50, 53, 54].
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Adding to the complexity, Strohschein et al. (2011) showed that Aqp4 deletion enhances gap-junctional coupling, which would facilitate K+ redistribution through the astroglial syncytium.
Enhanced gap junction conductance induced by rotigaptide decreased, while block by carbenoxolone facilitated the incidence of stretch-induced AF.
ACT1 redirects uncoupled Cx43 hemichannels into gap junctions, thereby reducing gap junction turnover and enhancing gap junction aggregation, without effecting Cx43 protein levels [ 33, 34].
Enhanced gap junction conductance induced by treatment with 100 1000 nM rotigaptide reduced SAF inducibility, and the gap junction blocker carbenoxolone increased SAF inducibility.
CaMKII has also been shown to mediate enhanced gap junctional coupling, mostly through Cx43, in response to high extracellular K+ in mouse spinal cord astrocytes [ 127].
Co-culturing also appears to enhance gap junctional intercellular communication as indicated by increased dye-coupled communication (Rojkind et al., 1995).
The effect of enhancing gap junction function by 100 1000 nM rotigaptide (ZP123) and block by 30 μM carbenoxolone on these parameters was measured.
Here, we first evaluated BT474 cells for ACT1 treatment-mediated effects on gap junction function by gap-FRAP and found that ACT1 treatment enhanced gap junction activity (Additional file 1: Figure S4A).
These findings indicate that MAK enhance gap junctional communication in liver of CH3-HeJ mice and may support previous in vitro findings which demonstrate that oxygen radical scavengers induce liver-specific cx expression in cultured hepatocytes [ 59].
Our data are compatible to the previous studies, indicating that 100 nM rotigaptide should be the best effective dose for enhancing gap junction conductance and preserving/ improving atrial conduction time.
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