UNC79:UNC80:NALCN transports Na+ extracellular region to cytosol

Stable Identifier
R-HSA-2730664
Type
Reaction [transition]
Species
Homo sapiens
Compartment
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The sodium leak channel non-selective protein NALCN, a nonselective cation channel, forms the background Na+ leak conductance and controls neuronal excitability (Lu et al. 2007, Ren 2011). Mice with mutant NALCN have a severely disrupted respiratory rhythm and die within 24 hours of birth. Calcium (Ca2+) influences neuronal excitability via the NALCN:UNC79:UNC80 complex, with high Ca2+ concentrations inhibiting transport of Na+ (Lu et al. 2010). Mutations in human NALCN lead to complex neurodevelopmental syndromes, including infantile hypotonia with psychomotor retardation and characteristic facies (IHPRF) and congenital contractures of limbs and face, hypotonia and developmental delay (CLIFAHDD) (Bouasse et al. 2019).

Literature References
PubMed ID Title Journal Year
21040849 Extracellular calcium controls background current and neuronal excitability via an UNC79-UNC80-NALCN cation channel complex

Lu, B, Zhang, Q, Wang, H, Wang, Y, Nakayama, M, Ren, D

Neuron 2010
17448995 The neuronal channel NALCN contributes resting sodium permeability and is required for normal respiratory rhythm

Lu, B, Su, Y, Das, S, Liu, J, Xia, J, Ren, D

Cell 2007
Participants
Output
Participates
Catalyst Activity

sodium channel activity of NALCN:UNC79:UNC80 [plasma membrane]

This event is regulated
Negatively by
Regulator
Orthologous Events
Cross References
Rhea
Authored
Reviewed
Created
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