Publication for SCN2A and SCN3A

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	SCN2A	sodium voltage-gated channel alpha subunit 2	6326			[link]
hsa	SCN3A	sodium voltage-gated channel alpha subunit 3	6328

Pubmed ID	Priority	Text
25360110	1.00	SCN2A, SCN3A, SCN5A, SCN6A, SCN9A, and SCN11A could be evidently shown in myenteric plexus of human colon in the majority of analyzed samples.
	0.94	SCN2A, SCN3A, SCN9A, and SCN11A, these sodium channel subtypes may have significant functional contributions to the excitability of specific populations of enteric neurons and alteration of them could be important in disease.
	0.87	SCN2A, SCN3A, SCN4A, SCN11A), which were present only in a few donors.
30531953	0.98	SCN2A, or SCN3A independently.
	0.97	SCN2A and SCN3A, that are located more distally to the SCN1A locus.
	0.95	SCN2A and more recently SCN3A are established monogenic causes of epileptic encephalopathy that, like SCN1A, cause dysfunction of the encoded ion-channels, which is believed to disturb the fine balance between neuronal excitation and inhibition.
	0.93	SCN2A, SCN3A, and TTC21B as the most likely genes underlying the signal at 2q24.3 for all epilepsy, focal epilepsy and genetic generalized epilepsy.
	0.91	SCN2A and SCN3A are associated with various epilepsy syndromes and mutations in TTC21B impair forebrain development.
30386239	0.98	Nav1.2-Nav1.3, Nav1.6, and Nav1.7.
	0.97	Nav1.2, Nav1.3, Nav1.6, and Nav1.7 channels but had negligible effect on Nav1.4, Nav1.5, Nav1.8, and Nav1.9 channels, suggesting that Ca2a is a selective antagonist of neuronal TTX-S VGSCs.
	0.91	Nav1.2 (IC50 of 216.3 +- 9.1 nM), Nav1.6 (IC50 of 313.6 +- 6.3 nM), and Nav1.3 (IC50 of 491.3 +- 3.9 nM) (Figure 2I).
	0.60	Nav1.2, Nav1.3, and Nav1.6 current amplitude by 82.6 +- 2.7%, 67.7 +- 3.8%, and 78.7 +- 2.9%, respectively.
31694722	0.98	SCN3A and resulted in a complete loss of SCN2A (Fig. 2, Table 3, Table 4).
	0.95	SCN3A, SCN2A, CSRNP3, GALNT3) and 121 kb (SCN1A), respectively.
	0.76	SCN2A also cause epileptic encephalopathy (MIM 613721) and missense variants in SCN3A have been implicated in focal epilepsy in children.
	0.60	SCN2A, and SCN3A, have been presented previously in cases with severe epileptic encephalopathies and developmental delay.
19763161	0.98	SCN2A have also been reported in patients with benign familial neonatal-infantile seizures and a single SCN3A mutation has recently been identified in a pediatric patient with partial epilepsy.
	0.97	SCN2A, SCN3A, SCN7A, KCNH7 or SLC4A10, all of which are candidate genes within the linkage region.
	0.81	SCN2A, SCN3A, SCN7A and SCN9A, ascertained by using the Agilent array comparative genomic hybridization platform, found no shared CNV between two affected K4425 individuals, III-12 and IV-9 (data not shown).
31904123	0.98	SCN2A,7 SCN3A,8 SCN8A,9 and SCN1B.10 Several other subunits, traditionally considered to be expressed at low levels in whole brain assays, have very restricted regional expression, for example, the "cardiac" sodium channel SCN5A within the limbic system11, 12 and may ultimately prove to play contributory roles (SCN4A,13, SCN5A,14 SCN7A,15 SCN9A,16 SCN10A17).
	0.94	Scn2a(1), Scn3a, and Scnb3 are expressed early and later decline in density, whereas Scn1a, Scn8a, Scn9a, and Scnb1, Scnb2, and Scnb4 are expressed predominantly at later ages.
	0.88	SCN2A subunit sodium channelopathy can coincide with larger scale cortical malformation.34, 35, 36 Cortical polymicrogyria has been described in cases with mutations in SCN3A, perhaps due to its early brain expression.37, 38
19005038	0.98	NaV1.3 channels are primarily localized in cell bodies, NaV1.2 channels in unmyelinated or pre-myelinated axons and dendrites, and NaV1.6 channels in myelinated axons and in dendrites.
	0.77	NaV1.2, NaV1.3, and NaV1.6 sodium channel subtypes, encoded by the SCN1A, SCN2A, SCN3A, and SCN8A genes, are the primary sodium channels in the central nervous system.
27956748	0.98	SCN2A, SCN3A and SCN8A) are associated with neurological, psychiatric and neurodevelopmental disorders including epilepsy, autism and cognitive impairment.
	0.95	SCN2A, SCN3A and SCN7A) and SCN1A is <200 kb away.
30314295	0.98	SCN2A is a member of the sodium channel family (consisting of fourteen members, including, SCN1A, SCN3A and SCN8A) that are widely expressed in neurons of the central nervous system (CNS) and implicated with seizure disorders.
19394292	0.97	SCN3A, but not SCN2A2, promoters depends on its SUMO-2 interaction motif.
	0.96	SCN2A2, and SCN3A mRNA levels were determined by RT-qPCR from HeLa cells transfected with 3xFLAG-SENP3-dN, 3xFLAG-SENP3-dN-C/S or 3xFLAG vector.
	0.96	SCN2A2 and SCN3A promoters by ChIP-qPCR.
	0.96	SCN2A2, SCN3A and CoREST1 transcripts were determined by RT-qPCR.
	0.95	SCN3A, but not the SCN2A2, promoters (Figure 6C).
	0.94	SCN2A2 and SCN3A.
	0.94	SCN2A2 and SCN3A promoters or RNA polymerase II polypeptide A exon (POLR2A ex).
	0.93	SCN2A2 and SCN3A were up-regulated in both CoREST1 and LSD1 stable knockdown cells.
	0.67	SCN3A promoters, while the SCN2A2 promoter was not occupied by SUMO-2/3 (Figure 6A and 6B).
	0.57	SCN3A genes, but did not affect another CoREST1/LSD1 target gene, SCN2A2.
23675382	0.97	SCN2A, SCN3A are highly expressed in neurons and glia throughout the central nervous system (CNS) and peripheral nervous system.
	0.97	SCN2A and SCN3A genes in a 25-year-old female with a history of infantile seizure, mental retardation, anxiety disorders, and neurobehavioral and psychiatric abnormalities.
	0.96	SCN2A and the non-coding exon 1a of SCN3A.
	0.95	SCN2A, SCN3A, SCN7A, and SCN9A genes form a 1.4-Mb SCN cluster on chromosome 2q24.3 .
	0.93	Nav1.2 and Nav1.3 amounts decrease during the second week of life .
	0.65	SCN2A and SCN3A in a patient with autistic features, developmental delay, language impairment, mental retardation, and dysmorphic features.
	0.65	SCN2A, and SCN3A genes are usually associated to epilepsy complicated by neurobehavioral comorbidities, which include cognitive impairment, psychiatric disorders, and social problems.
30071822	0.97	SCN2A2, SCN3A, GRB14 and COBLL1.
	0.97	SCN2A and non-coding exon 1a of SCN3A in a 25-year-old female with mental retardation, neurobehavioural and psychiatric abnormalities and a history of infantile seizures.
	0.95	SCN2A2, SCN3A and COBLL1 was reported in a patient with severe epilepsy.
	0.94	SCN2A and SCN3A deletion.
	0.86	SCN2A and SCN3A or GRB14, COBLL1 and SLC38A11, respectively, might also contribute to the development of tics, which remains subject to investigation in large hypothesis-driven association studies.
	0.74	SCN2A and SCN3A genes.
	0.63	SCN2A, SCN3A, GRB14, COBLL1 and SCL38A11 deletions with ASD and Tourette syndrome and possible implications for treatment.
27595042	0.97	SCN2A, and SCN3A:are all located on chromosome 2q24.
	0.86	SCN2A and SCN3A but not SCN1A can be associated with neonatal epilepsy and that they can present with a phenotype of a significant epileptic encephalopathy.
	0.82	SCN2A and SCN3A.
	0.80	SCN2A and SCN3A but not SCN1A had later onset of initial seizures at 3 months of age with eventual re-emergence of seizures later in childhood as well as intellectual disability at follow-up.
	0.71	SCN2A and SCN3A, but not SCN1A.
	0.67	SCN2A and SCN3A.
19806193	0.97	NaV1.2, NaV1.3, NaV1.6, and NaV1.7.
	0.87	NaV1.2, NaV1.3, NaV1.5, NaV1.6 and NaV1.7 in human cardiac fibroblasts.
	0.80	, NaV1.2, NaV1.3, NaV1.6, NaV1.7 (for INa.
	0.76	ol, NaV1.2/NaV1.3/NaV1.6/NaV1.7 for INa.
	0.74	NaV1.2, NaV1.3, NaV1.6 and NaV1.7 (for INa.
21962108	0.97	NaV1.2, 1.4 and 1.6, as well as NaV1.3 and 1.7.
	0.93	NaV1.2 and 1.4, we do not have an ideal basis for creating analogues selective for NaV1.3 and/or 1.7, so this will have to be pursued by creating a limited library of analogues of D9K13 and perhaps K9D13.
	0.64	NaV1.2, 1.4 and 1.6 and enhance activity against NaV1.3 and 1.7.
	0.59	NaV1.2, 1.4 and 1.6 could be modified to target the NaV1.3 and NaV1.7 subtypes.
27977115	0.97	SCN3A and SCN2A are two known target genes of LSD1 that have been studied in prior LSD1 gene expression studies.
	0.89	SCN2A and SCN3A was monitored after overexpression of wild type and K374R mutants and HDAC inhibitor treatment using a real time-polymerase chain reaction (RT-PCR).
	0.82	SCN3A and SCN2A are voltage-gated sodium channels that are aberrantly expressed in prostate cancers and are associated with metastasis, making them interesting biological targets.
	0.62	SCN2A (5.4 +- 1 fold, Figure S19) and SCN3A (2.4 +- 0.1 fold, Figure S19) compared to the DMSO control (Figures 6A and 7B, column 3 compared to column 2), which confirmed that LSD1-mediated gene expression is HDAC inhibitor-dependent.
18941776	0.97	NaV1.2 or NaV1.3 in CHO cells) or impediment of fast inactivation (right shift of voltage-dependence and faster recovery for cardiac > skeletal or neuronal NaV1.2 channels).
	0.84	NaV1.2 showing that co-expression of beta1 impedes slow inactivation; whereas an enhancement of slow inactivation by beta1 was reported for NaV1.4 (but no change for NaV1.5) in oocyes or for NaV1.2 and NaV1.3 in CHO cells.
	0.53	NaV1.2 and NaV1.3 in CHO cells have revealed a different loss-of-function gating defect, wherein the enhancement of fast inactivation by WT beta1 (-10 mV left shift and slower recovery) does not occur with C121W, which would thereby theoretically increase neuronal excitability.
22171219	0.97	Nav1.2, Nav1.3, Nav1.4, Nav1.5, Nav1.6, and Nav1.7 channels since these assays are sufficiently validated and quality control is followed rigorously.
	0.94	Nav1.2, Nav1.3, Nav1.4, Nav1.5, Nav1.6), and lamotrigine (Nav1.7).
	0.74	Nav1.2, Nav1.3, Nav1.4, Nav1.5, Nav1.6, and Nav1.7 assays collected over a 6 month period of time using IonWorks Quattro.
23639079	0.97	SCN2A (protein name: Nav1.2), SCN3A (Nav1.3), and SCN8A (Nav1.6) on iPSCs-derived neurons at 30 days of differentiation.
	0.93	SCN2A + SCN3A + SCN8A)/4 = 1.
	0.79	SCN2A expression was highest, followed by SCN1A, SCN3A, and SCN8A (Figure 2A and Additional file 2).
26728597	0.97	SCN2A, SCN3A, SCN4A, SCN5A, SCN9A, SCN10A, SCN1B, SCN2B, SCN3B, KCNN1, KCNJ5, KCNE1, KCNE2, KCNE3, KCND3, KCNQ1, KCNA5, KCNH2 and CACNA1C were endogenous expressed in HeLa cell lines (Fig. 1).
	0.93	SCN2A, SCN3A, SCN4A, SCN5A, SCN9A, SCN10A, SCN1B, SCN2B, SCN3B, KCNN1, KCNJ5, KCNE1, KCNE2, KCNE3, KCND3, KCNQ1, KCNA5, KCNH2 and CACNA1C.
	0.86	SCN2A, SCN3A, SCN4A, SCN5A, SCN9A, SCN10A, SCN1B, SCN2B, SCN3B, KCNN1, KCNJ5, KCNE1, KCNE2, KCNE3, KCND3, KCNQ1, KCNA5, KCNH2 and CACNA1C.
22412801	0.97	Nav1.2, Nav1.3, Nav1.4, Nav1.6, and Nav1.7 subtypes (TTX-sensitive VGSCs), whereas significantly higher (micromolar) concentrations are needed to block Nav1.5, Nav1.8 and Nav1.9 subtypes (TTX-resistant VGSCs).
	0.54	Nav1.2 was very recently identified as one of the sodium channel isoforms that mediate action potential firing in lamina I/II spinal cord neurons, which are primarily composed of Nav1.2 and Nav1.3 isoforms.
26503606	0.97	NaV1.2, NaV1.3, NaV1.5 and NaV1.6, and Lys methylation, which is included for NaV1.2 and NaV1.6.
	0.96	NaV1.2, NaV1.3, and NaV1.6.
28621020	0.97	SCN2A, SCN3A and SCN1A are inconsistent.
	0.97	SCN2A, and SCN9A (and potentially also SCN3A and SCN8A where splicing is conserved), this increase in function appears well-tolerated, and even appears strongly conserved in mammalian evolution.
30008854	0.97	Nav1.2, Nav1.3 (data not shown).
	0.92	Nav1.2, Nav1.3, and Nav1.6 subtypes are found in central nerve system.
19607678	0.97	SCN2A (also known as Nav1.2), SCN3A (also known as Nav1.3), SCN4A (also known as Nav1.4), SCN8A (also known as Nav1.6), and SCN9A (also known as Nav1.7).
21264295	0.97	Nav1.2, Nav1.3 and Nav1.6 are BmK IT2-insensitive, the action of BmK IT2 on Na+ currents of DRG neurons may be a result of selective modulation on other neuronal VGSC subtypes, most likely Nav1.7, Nav1.8 and/or Nav1.9 channels.
26991361	0.97	Nav1.2, Nav1.3, Nav1.7, and Nav1.5 subunits.
28235671	0.97	SCN2A, SCN3A, and SCN8A, which encode Nav1.1, Nav1.2, Nav1.3, and Nav1.6 respectively.
23702286	0.96	Nav1.2, Nav1.3, Nav1.4, Nav1.5, and Nav1.6 are all expressed in human atrial myocardium, but are localized in distinct patterns.
	0.95	Nav1.2, Nav1.3, Nav1.4 or Nav1.6 as well as the TTX-resistant Nav1.5 sodium channel expressed as normalized pixel density.
	0.93	Nav1.2, Nav1.3, and Nav1.4, and Nav1.6) in atrial muscle, in addition to the predominant TTX-resistant isoform Nav1.5.
	0.85	Nav1.2 for 2.5%, Nav1.3 for 0.4%, Nav1.4 for 2.6% and Nav1.6 for 4.4%.
30308978	0.96	NaV1.2 (n = 5), 426.3 +- 48.8 nM for NaV1.3 (n = 5), 290.1 +- 23.2 nM for NaV1.4 (n = 6), 478.0 +- 32.0 nM for NaV1.5 (n = 5), 158.6 +- 29.4 nM for NaV1.6 (n = 4), 188.9 +- 46.3 nM for NaV1.7 (n = 6), and 824.0 +- 68.7 nM for NaV1.8 (n = 5) (Figure 2I,J).
	0.94	NaV1.2 and NaV1.3 channels being the most affected (Figure 2A,B, inset).
	0.87	NaV1.2 and NaV1.3.
	0.80	NaV1.2, NaV1.3, NaV1.4, NaV1.5, NaV1.6, NaV1.7, and NaV1.8, respectively (n = 4-6).
26153865	0.96	Nav1.2, Nav1.3, Nav1.4, Nav1.5, Nav1.8, BgNav1 and DmNav1 (Figure 2, left panels).
28428547	0.95	NaV1.3, inhibits activation of NaV1.2, NaV1.6, and NaV1.7, and inhibits both activation and fast inactivation of NaV1.1, with no effect on NaV1.4 or NaV1.5 at sub-micromolar concentrations.
	0.89	NaV1.2, NaV1.3 and NaV1.7 (but not NaV1.1 or NaV1.6) are robustly expressed in the human neuroblastoma cell line, SH-SY5Y .
	0.62	NaV1.2 with ~70-fold selectivity over NaV1.3.
26035178	0.94	SCN2A and SCN3A were not significantly different between the naive SH-SY5Y cells (sham) and the stable-NAT SH-SY5Y cells (SCN1A expression could not be detected in the SH-SY5Y cell lines) (S5 Fig), further indicating that the functional effects of the NAT are SCN9A-specific.
	0.91	Nav1.2 or Nav1.3 in the NAT-stable SH-SY5Y cell line.
	0.87	SCN2A and SCN3A (S4 Fig).
18675520	0.94	Scn2a exons 17A, respectively, and within the SCN3A/locus424180 gene an 84 nt sequence shares 76% and 86% identities with the mouse and human Scn3a exons 17A, though no corresponding Scn3a exon 17B sequence was detected (Fig. 6).
	0.90	SCN2A and SCN3A are identical, as in the rat, and share 80% identity with exon 16A of SCN9A (Nav1.7).
26236192	0.94	Nav1.2, Nav1.3 and Nav1.6 channel subtypes are the primary Na+ channels in the CNS; by contrast, Nav1.7, Nav1.8 and Nav1.9 channel subtypes are mainly expressed in the peripheral nervous system (PNS); finally, Nav1.4 channels are expressed in skeletal muscle and Nav1.5 in the heart.
	0.87	Nav1.3 channels are primarily localized in cell bodies (Westenbroek et al.,), whereas Nav1.2 channels are positioned in unmyelinated or pre-myelinated axons and dendrites, and Nav1.6 channels in myelinated axons and dendrites (Caldwell et al.,).
30519187	0.93	Nav1.2, Nav1.3, Nav1.6, and Nav1.7) possess a CK2 serine/threonine kinase phosphorylation site downstream of the ankyrin G binding site in the II-III linker, that greatly increases affinity and required for the formation of stable ankyrin G - sodium channel complexes upon phosphorylation.
	0.91	Nav1.2, Nav1.3 and Nav1.7, are expressed primarily in central and peripheral nervous systems and are coded on human chromosome number 2 (linked to HOX D gene).
	0.62	Nav1.2, Nav1.3, Nav1.6, and Nav1.7 (Figure 11A).
	0.61	Nav1.2, Nav1.3, Nav1.6, and Nav1.7) possess a CK2 serine/threonine kinase phosphorylation site downstream of the ankyrin G binding site in the II-III linker (Figures 10, 11B), that greatly increases affinity and required for the formation of stable ankyrin G - sodium channel complexes upon phosphorylation.
26038700	0.92	NaV1.2: NaV1.3: NaV1.6: NaV1.7 = 1.00: 1.31: 1.37: 2.17: 1.15.
29735899	0.92	NaV1.2, NaV1.3, NaV1.4, NaV1.6 and NaV1.7.
24635129	0.91	hNav1.2, and hNav1.3 is not influenced; however, 100 muM rufinamide does alter the midpoint of hNav1.6 channel availability by approximately +5 mV (Figure 1 and Table 1).
	0.81	hNav1.2 (C), hNav1.3 (D), and hNav1.6 (E).
29335539	0.91	SCN2A, SCN3A, and SCN9A:are associated with a variety of monogenic childhood epilepsies such as DS in humans.
	0.88	SCN2A, SCN3A, and SCN9A.
25406007	0.89	NaV1.2, NaV1.3 or NaV1.7).
	0.65	NaV1.2, 1.3 nM, NaV1.3, 35 nM) (Figure 5).
	0.51	NaV1.2 and NaV1.3 (Figure 5)
28649286	0.89	SCN2A, and SCN3A sequencing, there was one affected individual with an SCN2A variant, which was absent in controls.
28168870	0.86	SCN2A, SCN4A, and SCN5A having the highest number of variants, whereas SCN3A and SCN11A have the fewest number of variants.
30146301	0.84	SCN3A mutations may activate different mechanisms than mutations in other VGSCs, like SCN1A, that are expressed postnatally, when both GOF and LOF are likely to modify excitability, altering circuit function, and SCN2A, where LOF (but not GOF) is reported in individuals with autism spectrum disorders without epilepsy.
28144265	0.80	SCN2A, SCN3A, SCN1B, SCN2B and epilepsy, SNP rs3812718 in the SCN1A gene showed the strongest correlation with all types of epilepsy (with or without febrile seizures).
27270488	0.78	SCN2A, and SCN3A are also implicated in a range of milder, self-limited neonatal and infantile epilepsy syndromes.
31947870	0.78	Nav1.2 (scn2a), Nav1.3 (scn3a) and Nav1.5 (scn5a) in MA.
22798951	0.77	NaV1.2, NaV1.3, and NaV1.6 isoforms are mainly expressed in the central nervous system (CNS).
	0.75	SCN2A, and SCN3A gene mutations may give rise to epilepsy and epileptic/convulsive disorders.
	0.55	NaV1.2, Nav1.3, Nav1.4, Nav1.6, and Nav1.7 isoforms.
25358543	0.71	Nav 1.2 mRNA and (B) Nav 1.3 mRNA.
29691040	0.63	SCN2A) gene is located on the positive strand of chromosome 2 (2q24.3) in humans, between the sodium channel gene SCN3A and the nuclear protein gene CSRNP3.
30744067	0.63	Nav1.3, and Nav1.6, BmK AEP also delays the inactivation kinetics of Nav1.2.
22125538	0.62	Nav1.2, Nav1.3, and Nav1.6 are widely expressed in the central nervous system (CNS) while Nav1.7, Nav1.8, and Nav1.9 are preferentially expressed in the peripheral nervous system (PNS; Black et al.,).
20831750	0.58	Nav1.2, Nav1.3 and Nav1.6), and four are expressed at high levels in the peripheral nervous system (Nav1.6, Nav1.7, Nav1.8 and Nav1.9).
29934975	0.57	SCN2A, SCN3A, and SCN9A) on chromosome 2 (Morrow et al., 2008; Table 3).
25294986	0.56	NaV1.2, and NaV1.6; we therefore could not exclude the possibility that the PC axon may express other channel subtypes, such as NaV1.3 and NaV1.5, that have been reported to be expressed in the mature cortex.