A Gain-of-Function Mutation inNALCNin a Child with Intellectual Disability, Ataxia, and Arthrogryposis

De Novo Mutations in NALCN Cause a Syndrome Characterized by Congenital Contractures of the Limbs and Face, Hypotonia, and Developmental Delay

(2015) Jessica X. Chong et al.   AMERICAN JOURNAL OF HUMAN GENETICS

The NCA sodium leak channel is required for persistent motor circuit activity that sustains locomotion

(2015) Shangbang Gao et al.   Nature Communications

De Novo Mutations in Moderate or Severe Intellectual Disability

(2014) Fadi F. Hamdan et al.   PLoS Genetics

Mutations in NALCN Cause an Autosomal-Recessive Syndrome with Severe Hypotonia, Speech Impairment, and Cognitive Delay

(2013) Moeenaldeen D. Al-Sayed et al.   AMERICAN JOURNAL OF HUMAN GENETICS

Recessive truncatingNALCNmutation in infantile neuroaxonal dystrophy with facial dysmorphism

(2013) Çiğdem Köroğlu et al.   JOURNAL OF MEDICAL GENETICS

NLF-1 Delivers a Sodium Leak Channel to Regulate Neuronal Excitability and Modulate Rhythmic Locomotion

(2013) Lin Xie et al.   NEURON

Extracellular Calcium Controls Background Current and Neuronal Excitability via an UNC79-UNC80-NALCN Cation Channel Complex

(2010) Boxun Lu et al.   NEURON

Failure of neuronal homeostasis results in common neuropsychiatric phenotypes

(2008) Melissa B. Ramocki et al.   NATURE

Genetic analysis of crawling and swimming locomotory patterns in C. elegans

(2008) J. T. Pierce-Shimomura et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

A Putative Cation Channel, NCA-1, and a Novel Protein, UNC-80, Transmit Neuronal Activity in C. elegans

(2008) Edward Yeh et al.   PLOS BIOLOGY