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The voltage‐gated sodium channel NaV1.7 is involved in various pain phenotypes and is physiologically regulated by the NaV‐β3‐subunit. Venom toxins ProTx‐II and OD1 modulate NaV1.7 channel function and may be useful as therapeutic agents and/or research tools. Here, we use patch‐clamp recordings to investigate how the β3‐subunit can influence and modulate the toxin‐mediated effects on NaV1.7 function,...
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