Ignet

Gene Information

Gene symbol: SCN5A

Gene name: sodium channel, voltage-gated, type V, alpha subunit

HGNC ID: 10593

Synonyms: Nav1.5, LQT3, HB1, HBBD, PFHB1, IVF, HB2, HH1, SSS1, CDCD2, CMPD2, ICCD

Related Genes

#	Gene Symbol	Number of hits
1	ACCN2	1 hits
2	AQP2	1 hits
3	AVP	1 hits
4	BSND	1 hits
5	CACNA1C	1 hits
6	CACNA1H	1 hits
7	CACNA2D1	1 hits
8	CACNB1	1 hits
9	CFTR	1 hits
10	CLCN2	1 hits
11	CTGF	1 hits
12	G6PC	1 hits
13	GRIK2	1 hits
14	KCNA2	1 hits
15	KCNA3	1 hits
16	KCNA4	1 hits
17	KCNA5	1 hits
18	KCNAB1	1 hits
19	KCNB1	1 hits
20	KCND1	1 hits
21	KCND3	1 hits
22	KCNE1	1 hits
23	KCNG2	1 hits
24	KCNH2	1 hits
25	KCNIP2	1 hits
26	KCNJ1	1 hits
27	KCNJ2	1 hits
28	KCNJ3	1 hits
29	KCNK3	1 hits
30	KCNN2	1 hits
31	KCNQ1	1 hits
32	KCNQ4	1 hits
33	LDLR	1 hits
34	NR3C2	1 hits
35	ORAI1	1 hits
36	PHOX2B	1 hits
37	SCARB1	1 hits
38	SCN1B	1 hits
39	SGK1	1 hits
40	STIM1	1 hits

Related Sentences

#	PMID	Sentence
1	11026758	Liver lipid parameters were measured and lipoprotein receptors (LDLr, SR-BI and HB2) were assayed by immunodetection.
2	11026758	The expression of LDLr and HB2 was unchanged at day 6, but was significantly modified at day 28 (+140% for LDLr and -50% for HB2).
3	11026758	Liver lipid parameters were measured and lipoprotein receptors (LDLr, SR-BI and HB2) were assayed by immunodetection.
4	11026758	The expression of LDLr and HB2 was unchanged at day 6, but was significantly modified at day 28 (+140% for LDLr and -50% for HB2).
5	16159898	Aldosterone increases urine production and decreases apical AQP2 expression in rats with diabetes insipidus.
6	16159898	We investigated the effects of 7-day aldosterone infusion or oral spironolactone treatment on water balance and aquaporin (AQP) 2 expression in rats with 21 days of lithium-induced nephrogenic diabetes insipidus (Li-NDI).
7	16159898	Semiquantitative confocal immunofluorescence microscopy of AQP2 immunolabeling showed reduced AQP2 expression in the apical plasma membrane domain in connecting tubule (CNT) and initial cortical collecting ducts (iCCD) in response to aldosterone-treated rats compared with rats treated with lithium only.
8	16159898	Spironolactone significantly increased apical AQP2 expression in the iCCD compared with rats treated with lithium only.
9	16159898	We also tested whether similar changes could be observed in vasopressin-deficient BB rats and found similar changes in urine production and subcellular AQP2 expression in the CNT and iCCD in response to aldosterone and spironolactone.
10	16159898	This study shows that aldosterone treatment perturbs diabetes insipidus and is associated with AQP2 redistribution in CNT and iCCD likely mediated by the spironolactone-sensitive mineralocorticoid receptor.
11	16159898	Aldosterone increases urine production and decreases apical AQP2 expression in rats with diabetes insipidus.
12	16159898	We investigated the effects of 7-day aldosterone infusion or oral spironolactone treatment on water balance and aquaporin (AQP) 2 expression in rats with 21 days of lithium-induced nephrogenic diabetes insipidus (Li-NDI).
13	16159898	Semiquantitative confocal immunofluorescence microscopy of AQP2 immunolabeling showed reduced AQP2 expression in the apical plasma membrane domain in connecting tubule (CNT) and initial cortical collecting ducts (iCCD) in response to aldosterone-treated rats compared with rats treated with lithium only.
14	16159898	Spironolactone significantly increased apical AQP2 expression in the iCCD compared with rats treated with lithium only.
15	16159898	We also tested whether similar changes could be observed in vasopressin-deficient BB rats and found similar changes in urine production and subcellular AQP2 expression in the CNT and iCCD in response to aldosterone and spironolactone.
16	16159898	This study shows that aldosterone treatment perturbs diabetes insipidus and is associated with AQP2 redistribution in CNT and iCCD likely mediated by the spironolactone-sensitive mineralocorticoid receptor.
17	16159898	Aldosterone increases urine production and decreases apical AQP2 expression in rats with diabetes insipidus.
18	16159898	We investigated the effects of 7-day aldosterone infusion or oral spironolactone treatment on water balance and aquaporin (AQP) 2 expression in rats with 21 days of lithium-induced nephrogenic diabetes insipidus (Li-NDI).
19	16159898	Semiquantitative confocal immunofluorescence microscopy of AQP2 immunolabeling showed reduced AQP2 expression in the apical plasma membrane domain in connecting tubule (CNT) and initial cortical collecting ducts (iCCD) in response to aldosterone-treated rats compared with rats treated with lithium only.
20	16159898	Spironolactone significantly increased apical AQP2 expression in the iCCD compared with rats treated with lithium only.
21	16159898	We also tested whether similar changes could be observed in vasopressin-deficient BB rats and found similar changes in urine production and subcellular AQP2 expression in the CNT and iCCD in response to aldosterone and spironolactone.
22	16159898	This study shows that aldosterone treatment perturbs diabetes insipidus and is associated with AQP2 redistribution in CNT and iCCD likely mediated by the spironolactone-sensitive mineralocorticoid receptor.
23	16159898	Aldosterone increases urine production and decreases apical AQP2 expression in rats with diabetes insipidus.
24	16159898	We investigated the effects of 7-day aldosterone infusion or oral spironolactone treatment on water balance and aquaporin (AQP) 2 expression in rats with 21 days of lithium-induced nephrogenic diabetes insipidus (Li-NDI).
25	16159898	Semiquantitative confocal immunofluorescence microscopy of AQP2 immunolabeling showed reduced AQP2 expression in the apical plasma membrane domain in connecting tubule (CNT) and initial cortical collecting ducts (iCCD) in response to aldosterone-treated rats compared with rats treated with lithium only.
26	16159898	Spironolactone significantly increased apical AQP2 expression in the iCCD compared with rats treated with lithium only.
27	16159898	We also tested whether similar changes could be observed in vasopressin-deficient BB rats and found similar changes in urine production and subcellular AQP2 expression in the CNT and iCCD in response to aldosterone and spironolactone.
28	16159898	This study shows that aldosterone treatment perturbs diabetes insipidus and is associated with AQP2 redistribution in CNT and iCCD likely mediated by the spironolactone-sensitive mineralocorticoid receptor.
29	20004937	Post-mortem heart sections were immunohistochemically stained for collagen types I and III and connective tissue growth factor (CTGF).
30	20004937	Genomic DNA was prepared from post-mortem samples, and genetic analysis was performed in the SCN5A, G6PC, PHOX2B, and CTGF genes.
31	20004937	Twenty-two dead in bed syndrome cases were identified and staining of heart sections for collagen I and III, and CTGF showed no differences between dead in bed syndrome cases and controls.
32	20004937	No genetic variants were found in G6PC, PHOX2B, and CTGF, and dead in bed syndrome cases were not associated with the G-945C CTGF promoter polymorphism.
33	22581745	Expression of genes encoding cardiac muscle proteins (Myh6/7, Mybpc3, Myl1/3, Actc1, Tnni3, Tnn2, Tpm1/2/4 and Dbi) and intercellular proteins (Gja1/4/5/7, Dsp and Cav1/3) were unaltered in GK ventricle compared with control ventricle.
34	22581745	The expression of genes encoding some membrane pumps and exchange proteins was unaltered (Atp1a1/2, Atp1b1 and Slc8a1), whilst others were either upregulated (Atp1a3, relative expression 2.61 ± 0.69 versus 0.84 ± 0.23) or downregulated (Slc9a1, 0.62 ± 0.07 versus 1.08 ± 0.08) in GK ventricle compared with control ventricle.
35	22581745	The expression of genes encoding some calcium (Cacna1c/1g, Cacna2d1/2d2 and Cacnb1/b2), sodium (Scn5a) and potassium channels (Kcna3/5, Kcnj3/5/8/11/12, Kchip2, Kcnab1, Kcnb1, Kcnd1/2/3, Kcne1/4, Kcnq1, Kcng2, Kcnh2, Kcnk3 and Kcnn2) were unaltered, whilst others were either upregulated (Cacna1h, 0.95 ± 0.16 versus 0.47 ± 0.09; Scn1b, 1.84 ± 0.16 versus 1.11 ± 0.11; and Hcn2, 1.55 ± 0.15 versus 1.03 ± 0.08) or downregulated (Hcn4, 0.16 ± 0.03 versus 0.37 ± 0.08; Kcna2, 0.35 ± 0.03 versus 0.80 ± 0.11; Kcna4, 0.79 ± 0.25 versus 1.90 ± 0.26; and Kcnj2, 0.52 ± 0.07 versus 0.78 ± 0.08) in GK ventricle compared with control ventricle.
36	23012321	SGK1 is activated by insulin and growth factors through PI3K and 3-phosphoinositide-dependent kinase PDK1.
37	23012321	SGK1 activates a wide variety of ion channels (e.g., ENaC, SCN5A, TRPV4-6, ROMK, Kv1.3, Kv1.5, Kv4.3, KCNE1/KCNQ1, KCNQ4, ASIC1, GluR6, ClCKa/barttin, ClC2, CFTR, and Orai/STIM), which participate in the regulation of transport, hormone release, neuroexcitability, inflammation, cell proliferation, and apoptosis.
38	23933686	SGK1 is activated by insulin and growth factors via phosphatidylinositol-3-kinase, 3-phosphoinositide dependent-kinase PDK1, and mTOR.
39	23933686	NCC, NKCC, NHE1, NHE3, SGLT1, several amino acid transporters) and many ion channels (e.g.
40	23933686	ENaC, SCN5A, TRPV4-6, Orai1/STIM1, ROMK, KCNE1/KCNQ1, GluR6, CFTR).
41	23933686	SGK1 further up-regulates a number of enzymes (e.g. glycogen-synthase-kinase-3, ubiquitin-ligase Nedd4-2), and transcription factors (e.g. forkhead-transcription-factor FOXO3a, β-catenin, nuclear-factor-kappa-B NFκB).