NALCN / ATTO 488 / S187-7
Product Details
| Description | Mouse monoclonal to NALCN (ATTO-488). NALCN (sodium leak channel non-selective protein), alsoknown as CanIon or VGCNL1 (voltage gated channel-like protein 1), is a 1738 amino acid multi-pass membrane protein that belongs to the cation-nonselective channel family. NALCN is highly conserved in mammals and is widely expressed in the central nervous system. Activated by NK-1R, NALCN is a voltage-independent, nonselective cation channel which is permeable to sodium, potassium and calcium ions. NALCN is responsible for background sodium ion leak conductance in neurons and regulates basal excitability of the nervous systems. Defects of NALCN in mice causes disruption in respiratory rhythm and death occurs within 24 hours of birth. Three isoforms of NALCN exists due to alternative splicing events.. - | |
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| Conjugate | ATTO 488 | |
| Clone | S187-7 | |
| Target Species | Human, Mouse, Rat | |
| Applications | ICC, WB | |
| Supplier | Biorbyt | |
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About NALCN
This gene encodes a voltage-independent, nonselective cation channel which belongs to a family of voltage-gated sodium and calcium channels that regulates the resting membrane potential and excitability of neurons. This family is expressed throughout the nervous system and conducts a persistent sodium leak current that contributes to tonic neuronal excitability. The encoded protein forms a channelosome complex that includes G-protein-coupled receptors, UNC-79, UNC-80, NCA localization factor-1, and src family tyrosine kinases. Naturally occurring mutations in this gene are associated with infantile neuroaxonal dystrophy, infantile hypotonia with psychomotor retardation and characteristic facies (IHPRF) syndrome, and congenital contractures of the limbs and face with hypotonia and developmental delay (CLIFAHDD) syndrome. A knockout of the orthologous gene in mice results in paralysis with a severely disrupted respiratory rhythm, and lethality within 24 hours after birth. [provided by RefSeq, Apr 2017]
This gene encodes a voltage-independent, nonselective cation channel which belongs to a family of voltage-gated sodium and calcium channels that regulates the resting membrane potential and excitability of neurons. This family is expressed throughout the nervous system and conducts a persistent sodium leak current that contributes to tonic neuronal excitability. The encoded protein forms a channelosome complex that includes G-protein-coupled receptors, UNC-79, UNC-80, NCA localization factor-1, and src family tyrosine kinases. Naturally occurring mutations in this gene are associated with infantile neuroaxonal dystrophy, infantile hypotonia with psychomotor retardation and characteristic facies (IHPRF) syndrome, and congenital contractures of the limbs and face with hypotonia and developmental delay (CLIFAHDD) syndrome. A knockout of the orthologous gene in mice results in paralysis with a severely disrupted respiratory rhythm, and lethality within 24 hours after birth. [provided by RefSeq, Apr 2017]
About ATTO 488
ATTO 488 is from ATTO-Tec Gmbh has an excitation peak at 501 nm and an emission peak at 523 nm.
ATTO 488 is from ATTO-Tec Gmbh has an excitation peak at 501 nm and an emission peak at 523 nm.
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113 NALCN antibodies from over 10 suppliers available with over 35 conjugates.
