Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, United States.
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan, United States.
Am J Physiol Cell Physiol. 2023 Mar 1;324(3):C694-C706. doi: 10.1152/ajpcell.00335.2022. Epub 2023 Jan 30.
The inward rectifier potassium channel Kir7.1, encoded by the gene, is a tetramer composed of two-transmembrane domain-spanning monomers, closer in homology to Kir channels associated with potassium transport such as Kir1.1, 1.2, and 1.3. Compared with other channels, Kir7.1 exhibits small unitary conductance and low dependence on external potassium. Kir7.1 channels also show a phosphatidylinositol 4,5-bisphosphate (PIP) dependence for opening. Accordingly, retinopathy-associated Kir7.1 mutations mapped at the binding site for PIP resulted in channel gating defects leading to channelopathies such as snowflake vitreoretinal degeneration and Leber congenital amaurosis in blind patients. Lately, this channel's role in energy homeostasis was reported due to the direct interaction with the melanocortin type 4 receptor (MC4R) in the hypothalamus. As this channel seems to play a multipronged role in potassium homeostasis and neuronal excitability, we will discuss what is predicted from a structural viewpoint and its possible implications for hunger control.
内向整流钾通道 Kir7.1 由 基因编码,是由两个跨膜结构域贯穿单体组成的四聚体,与与钾转运相关的 Kir 通道(如 Kir1.1、1.2 和 1.3)更具同源性。与其他通道相比,Kir7.1 表现出较小的单通道电导和对外部钾的低依赖性。Kir7.1 通道也表现出对磷脂酰肌醇 4,5-二磷酸 (PIP) 开放的依赖性。因此,与视网膜病变相关的 Kir7.1 突变定位于 PIP 的结合位点,导致通道门控缺陷,导致通道病,如雪花状玻璃体视网膜变性和盲患者的先天性黑蒙 Leber。最近,由于在下丘脑与黑皮质素 4 型受体 (MC4R) 的直接相互作用,该通道在能量稳态中的作用被报道。由于该通道似乎在钾稳态和神经元兴奋性中发挥多方面作用,我们将从结构角度讨论其可能的预测及其对饥饿控制的影响。