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Proposed model of the function of KCNB1‐LepR complexes in ARHPOMC neurons. In WT cells, the conducting functions of the channel modulate neuron excitability. In addition, the allosteric changes associated with the opening/closing of KCNB1 are translated to the LepR modulating its function. When the channel is missing, like in NULL neurons, in addition to abnormal depolarization, the function of the LepR is impaired resulting in dysregulated POMC production.
