IndraLab

Statements


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sparser
"Oxidative stress also affects I Na by modulating the expression of the major in the heart, Na V 1.5 encoded by SCN5A . Ang II and H 2 O 2 promote the binding of NF-kB to the cardiac Scn5a promoter, reducing Scn5a mRNA levels [ xref ]."

sparser
"H 2 O 2 and angiotensin II (AngII) downregulate a cardiac Na + channel (SCN5A) transcription in isolated ventricular myocytes through NF-κB binding to SCN5A promoter, resulting in arrhythmia by reducing the total sodium current and slowing the CV xref ."

sparser
"Treatment of cardiomyocytes with angiotensin II (Ang II) or hydrogen peroxide led to increased binding of NF-κB to the SCN5A promoter and subsequently decreased transcriptional activity."

sparser
"Elevated angiotensin II levels and the increased oxidative stress increase NF-κB binding to the SCN5A promoter region, thereby decreasing its transcriptional activity (Shang et al., xref )."

reach
"Angiotensin II (AngII) or H 2 O 2 treatment of cardiomyocytes results in increased NF-kappaB binding to SCN5A promoter with subsequent reduction in transcriptional activity [XREF_BIBR]."

sparser
"This is in agreement with another study xref that demonstrated that NFκB can directly bind to the SCN5A promoter, which is involved in down-transcription of the Na v 1.5 channel in rat ventricular cells."

sparser
"NF-κB bound to the SCN5A promoter region [179] and reduced Nav1.5 expression and I Na density in H9c2 myocytes [180] ."

sparser
"Angiotensin II (AngII) or H 2 O 2 treatment of cardiomyocytes results in increased NF-κB binding to SCN5A promoter with subsequent reduction in transcriptional activity [ xref ]."