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Article

Intellectual disability-associated UNC80 mutations reveal inter-subunit interaction and dendritic function of the NALCN channel complex.

Nature communications - 3 Jul 2020

Wie Jinhong, Bharthur Apoorva, Wolfgang Morgan, Narayanan Vinodh, Ramsey Keri, Aranda Kimberly, Zhang Qi, Zhou Yandong, Ren Dejian

Abstract excerpt

The sodium-leak channel NALCN forms a subthreshold sodium conductance that controls the resting membrane potentials of neurons. The auxiliary subunits of the channel and their functions in mammals are largely unknown. In this study, we demonstrate that two large proteins UNC80 and UNC79 are subunits of the NALCN complex. UNC80 knockout mice are neonatal lethal. The C-terminus of UNC80 contains a domain that...

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Identifiers

PMID: 32620897
DOI: 10.1038/s41467-020-17105-8
PMCID: PMC7335163

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Intellectual disability-associated UNC80 mutations reveal inter-subunit interaction and dendritic function of the NALCN channel complex.PMID 32620897Read ↗

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