IndraLab

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AntagoNAT activates SCN1A. 4 / 4
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"Overall, these results indicate that AntagoNAT mediated inhibition of SCN1ANAT results in the upregulation of SCN1A regardless of the SCN1A mutation type, thus increasing potential applicability of the AntagoNAT method in the treatment of Dravet syndrome and other diseases caused by de-novo mutations."
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"While AntagoNAT treatment upregulated SCN1A, it did not affect> 90% of all expressed genes, including other highly homologous sodium channel subunits and genes immediately adjacent to SCN1A on the chromosome (XREF_FIG; XREF_SUPPLEMENTARY)."
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"Taken together, our results demonstrate that at least some of the major aspects of Dravet are likely to be caused by persistent SCN1A deficit after birth and can be improved by AntagoNAT mediated upregulation of SCN1A."
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"Taken together, these experiments demonstrated that AntagoNAT mediated increase of Scn1a in adult Dravet mice (Scn1a E1099X/+) can improve spontaneous seizure phenotype."
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