Calmodulin Independent Kv7.2 Activity
Author Information
Author(s): Gómez-Posada Juan Camilo, Aivar Paloma, Alberdi Araitz, Alaimo Alessandro, Etxeberría Ainhoa, Fernández-Orth Juncal, Zamalloa Teresa, Roura-Ferrer Meritxell, Villace Patricia, Areso Pilar, Casis Oscar, Villarroel Alvaro
Primary Institution: Unidad de Biofísica, Consejo Superior de Investigaciones Científicas-Universidad del País Vasco/Euskal Herriko Unibersitatea, Leioa, Spain
Hypothesis
Can Kv7 channels function without the constitutive tethering of calmodulin?
Conclusion
The study reveals that Kv7 channels can function independently of calmodulin binding.
Supporting Evidence
- Mutations in Kv7.2 that disrupt calmodulin binding cause Benign Familial Neonatal Convulsions.
- The S511D mutation allows Kv7.2 to function without calmodulin.
- Calmodulin is not required for Kv7 channel function as previously thought.
Takeaway
This study shows that a specific mutation allows a potassium channel to work without needing a helper protein called calmodulin.
Methodology
The researchers used yeast two-hybrid systems and electrophysiological recordings in Xenopus oocytes to study the function of Kv7.2 channels with specific mutations.
Limitations
The study primarily focuses on a specific mutation and may not generalize to all Kv7 channels or other conditions.
Digital Object Identifier (DOI)
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