A novel Kir7.1 splice variant expressed in various mouse tissues shares organisational and functional properties with human Leber amaurosis-causing mutations of this K+ channel

Author:

Vera Erwin,Cornejo Isabel,Burgos Johanna,Niemeyer María Isabel,Sepúlveda Francisco V.,Cid L. Pablo

Funder

FONDECYT

Centro de Estudios Científicos (CECs)

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

Cited by 6 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. The unique structural characteristics of the Kir 7.1 inward rectifier potassium channel: a novel player in energy homeostasis control;American Journal of Physiology-Cell Physiology;2023-03-01

2. The cellular pathways that maintain the quality control and transport of diverse potassium channels;Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms;2023-03

3. Inward rectifier potassium (Kir) channels in the retina: living our vision;American Journal of Physiology-Cell Physiology;2022-09-01

4. Kir7.1 disease mutant T153I within the inner pore affects K+ conduction;American Journal of Physiology-Cell Physiology;2022-07-01

5. Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications;Pharmacology of Potassium Channels;2021

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