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Recombinant Rat Sodium channel protein type 1 subunit alpha (Scn1a), partial

Recombinant Rat Sodium channel protein type 1 subunit alpha (Scn1a), partial

Code
MSDS	MSDS Datasheet
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Source
Conjugate
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Target Background

Product Details

Purity

>85% (SDS-PAGE)

Target Names

Scn1a

Uniprot NO.

P04774

Alternative Names

Scn1a; Sodium channel protein type 1 subunit alpha; Sodium channel protein brain I subunit alpha; Sodium channel protein type I subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.1

Species

Rattus norvegicus (Rat)

Source

Yeast

Protein Length

Partial

Tag Info

N-terminal His-tagged/Tag-Free
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.

Storage Condition

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.

Shelf Life

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.

Notes

Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

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Target Background

Function(From Uniprot)

Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. Plays a key role in brain, probably by regulating the moment when neurotransmitters are released in neurons. Involved in sensory perception of mechanical pain: activation in somatosensory neurons induces pain without neurogenic inflammation and produces hypersensitivity to mechanical, but not thermal stimuli.

Gene References into Functions

Nav1.1 in facilitates fast-firing properties in medial septum neurons. Nav1.1 deficits may disrupt information processing in Dravet syndrome via a dysregulation of theta wave brain rhythms. PMID:26978272
Scn1a mutant rats demonstrate a higher hyperthermia-induced seizure susceptibility than wild type rats. PMID:23375560
Hyperthermia-induced seizures occurred in Scn1a mutant rats at high-frequency electroencephalographic oscillations. PMID:22920678
We show that reduction of Nav1.1 expression in the medial septum and diagonal band of Broca leads to a dysregulation of hippocampal oscillations in association with a spatial memory deficit PMID:23318929
In the dorsal horn of the developing rat, Na(v) isoforms are developmentally regulated at the mRNA level in a subtype-specific manner, as Na(v)1.2 and Na(v)1.3 decreased significantly from P3 to adulthood, while Na(v)1.1 was upregulated during this period PMID:23219908
Identification of the cysteine residue responsible for disulfide linkage of Na+ channel alpha and beta2 subunits PMID:22992729
Results suggest that an early increase in dorsal root ganglion Nav1.1 expression after peripheral nerve injury might be involved in the induction of neuropathic pain. PMID:21714116
Hyperthermia-induced seizure-susceptible rats are associated with febrile seizures and display the hyperexcitability of limbic neurons associated with the Scn1a missense mutation. PMID:20875856
An important mechanism of electroacupuncture therapy is its regulation of Nav1.6 and Nav1.1 expression after ischemia. PMID:20483028
Scn1a missense mutation preferentially impairs GABA(A) receptor-mediated synaptic transmission without directly altering the excitability of the pyramidal neurons in the hippocampus, which may be linked to the pathogenesis of febrile seizures. PMID:20707984
TTX-sensitive sodium channel alpha-subunit isoforms Na(v)1.1, Na(v)1.2, Na(v)1.3, Na(v)1.4 and Na(v)1.6 were detected in neonatal rat heart but at levels reduced compared to the predominant cardiac alpha-subunit isoform, Na(v)1.5. PMID:19426735
Quantitative and relative changes in expression of NaCh genes in neurons following injury produced by selective activation of voltage-gated sodium channels. Gene Nav1.1. may play role in neuronal injury/recovery process. PMID:12835125
A novel site of high-density sodium channel clustering in the inner plexiform layer of the retina is described, marked by ankyrin-G and neurofascin. PMID:15797713
these data map the time-dependent loss of Na(v)1.1 mRNA and protein following focal ischemic brain injury PMID:15878599
Na(V)1.1 was distributed in a similar manner to Na(V)1.5: atrial & ventricular myocardium & the left bundle branch, the inferior nodal extension & transitional zone. PMID:16966585
Results suggest that transient cerebral ischemia renders CA1 interneurons less excitable, that depressed excitability involves impaired Na(+) channel activation and that Na(+) channel dysfunction is explained by reduced expression of the Na(v)1.1 subunit. PMID:17228331
This study combined ISH with immunohistochemistry and discovered that most of the PV-immunoreactive cells located at the INL/IPL border express Nav1.1. Our results show that AII amacrine cells express Nav1.1. PMID:17709186