Ignet

Gene Information

Gene symbol: SLC9A3

Gene name: solute carrier family 9, subfamily A (NHE3, cation proton antiporter 3), member 3

HGNC ID: 11073

Related Genes

#	Gene Symbol	Number of hits
1	ACO2	1 hits
2	AQP1	1 hits
3	AQP2	1 hits
4	COL1A1	1 hits
5	COL4A4	1 hits
6	EGFR	1 hits
7	FAM20C	1 hits
8	HBB	1 hits
9	INS	1 hits
10	MAPK3	1 hits
11	NOS3	1 hits
12	SILV	1 hits
13	SLC12A1	1 hits
14	SLC12A3	1 hits
15	SLC5A1	1 hits
16	SLC5A2	1 hits
17	SLC9A1	1 hits
18	SLC9A3R2	1 hits
19	SLC9A4	1 hits

Related Sentences

#	PMID	Sentence
1	9288535	However, there is no evidence that there is expression of NHE-3 or NHE-4 in peripheral blood cells.
2	10966935	The changes in whole kidney expression of aquaporin-1 (AQP1), -2, and -3 as well as Na-K-ATPase, type 3 Na/H exchanger (NHE3), type 2 Na-Pi cotransporter (NaPi-2), type 1 bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1), and thiazide-sensitive Na-Cl cotransporter (TSC) were examined in rats treated with Li orally for 4 wk: protocol 1, high doses of Li (high Na(+) intake), and protocol 2, low doses of Li (identical food and normal Na(+) intake in Li-treated and control rats).
3	10966935	Immunoelectron microscopy confirmed the dramatic downregulation of AQP2 and AQP3, whereas AQP4 labeling was not reduced.
4	10966935	However, the expression of several major Na(+) transporters in the proximal tubule, loop of Henle, and distal convoluted tubule was unchanged in protocol 2, whereas in protocol 1 significantly increased NHE3 and BSC-1 expression or reduced NaPi-2 expression was associated with chronic Li treatment.
5	10966935	In conclusion, severe downregulation of AQP2 and AQP3 appears to be important for the development of Li-induced polyuria.
6	10966935	In contrast, the increased or unchanged expression of NHE3, BSC-1, Na-K-ATPase, and TSC indicates that these Na(+) transporters do not participate in the development of Li-induced polyuria.
7	10966935	The changes in whole kidney expression of aquaporin-1 (AQP1), -2, and -3 as well as Na-K-ATPase, type 3 Na/H exchanger (NHE3), type 2 Na-Pi cotransporter (NaPi-2), type 1 bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1), and thiazide-sensitive Na-Cl cotransporter (TSC) were examined in rats treated with Li orally for 4 wk: protocol 1, high doses of Li (high Na(+) intake), and protocol 2, low doses of Li (identical food and normal Na(+) intake in Li-treated and control rats).
8	10966935	Immunoelectron microscopy confirmed the dramatic downregulation of AQP2 and AQP3, whereas AQP4 labeling was not reduced.
9	10966935	However, the expression of several major Na(+) transporters in the proximal tubule, loop of Henle, and distal convoluted tubule was unchanged in protocol 2, whereas in protocol 1 significantly increased NHE3 and BSC-1 expression or reduced NaPi-2 expression was associated with chronic Li treatment.
10	10966935	In conclusion, severe downregulation of AQP2 and AQP3 appears to be important for the development of Li-induced polyuria.
11	10966935	In contrast, the increased or unchanged expression of NHE3, BSC-1, Na-K-ATPase, and TSC indicates that these Na(+) transporters do not participate in the development of Li-induced polyuria.
12	12904328	In study 1, STZ treatment resulted in significantly increased band densities for the type 3 sodium/hydrogen exchanger (NHE3), the thiazide-sensitive Na-Cl cotransporter (NCC), and epithelial sodium channel (ENaC) subunits alpha, beta, and gamma (85- and 70-kDa bands) to 204, 125, 176, 132, 147, and 241% of vehicle mean, respectively.
13	12904328	In study 2, aquaporin-2 (AQP2) and AQP3 were increased with DM, but not AQP1 or AQP4.
14	12904328	Whole kidney abundance of AQP3, the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), and gamma-ENaC (85-kDa band) correlated most strongly with blood glucose in study 3.
15	18417539	A lower dose of fatty acids that leads to intracellular lipid accumulation but does not change baseline NHE3 is sufficient to abolish the stimulation of NHE3 by insulin and to partially block the stimulation of NHE3 by glucocorticoid hormones; acid regulation of NHE3 in lipid-loaded OKP cells is not affected.
16	20003708	Effect of potent redox-modulating manganese porphyrin, MnTM-2-PyP, on the Na(+)/H(+) exchangers NHE-1 and NHE-3 in the diabetic rat.
17	20003708	NHE-1 and NHE-3 isoform expression, Na(+),K(+)-ATPase activity, and markers of ROS/RNS-induced damage were determined in kidney homogenates.
18	20003708	Diabetes caused lipid peroxidation, inactivation of aconitase, and increase of nitrotyrosine, which paralleled an increase in NHE-1 and NHE-3 expression and Na(+),K(+)-ATPase activity.
19	20003708	MnTM-2-PyP treatment had no effect on blood glucose and glycosylated hemoglobin, but suppressed lipid peroxidation and nitrotyrosine, protected aconitase against inactivation, and reversed the induction of NHE-1 and NHE-3 isoforms.
20	20003708	Mn(III) alkylpyridylporphyrins were previously found to inhibit activation of major transcription factors, including SP-1 via scavenging of signaling ROS/RNS.
21	20003708	Effect of potent redox-modulating manganese porphyrin, MnTM-2-PyP, on the Na(+)/H(+) exchangers NHE-1 and NHE-3 in the diabetic rat.
22	20003708	NHE-1 and NHE-3 isoform expression, Na(+),K(+)-ATPase activity, and markers of ROS/RNS-induced damage were determined in kidney homogenates.
23	20003708	Diabetes caused lipid peroxidation, inactivation of aconitase, and increase of nitrotyrosine, which paralleled an increase in NHE-1 and NHE-3 expression and Na(+),K(+)-ATPase activity.
24	20003708	MnTM-2-PyP treatment had no effect on blood glucose and glycosylated hemoglobin, but suppressed lipid peroxidation and nitrotyrosine, protected aconitase against inactivation, and reversed the induction of NHE-1 and NHE-3 isoforms.
25	20003708	Mn(III) alkylpyridylporphyrins were previously found to inhibit activation of major transcription factors, including SP-1 via scavenging of signaling ROS/RNS.
26	20003708	Effect of potent redox-modulating manganese porphyrin, MnTM-2-PyP, on the Na(+)/H(+) exchangers NHE-1 and NHE-3 in the diabetic rat.
27	20003708	NHE-1 and NHE-3 isoform expression, Na(+),K(+)-ATPase activity, and markers of ROS/RNS-induced damage were determined in kidney homogenates.
28	20003708	Diabetes caused lipid peroxidation, inactivation of aconitase, and increase of nitrotyrosine, which paralleled an increase in NHE-1 and NHE-3 expression and Na(+),K(+)-ATPase activity.
29	20003708	MnTM-2-PyP treatment had no effect on blood glucose and glycosylated hemoglobin, but suppressed lipid peroxidation and nitrotyrosine, protected aconitase against inactivation, and reversed the induction of NHE-1 and NHE-3 isoforms.
30	20003708	Mn(III) alkylpyridylporphyrins were previously found to inhibit activation of major transcription factors, including SP-1 via scavenging of signaling ROS/RNS.
31	20003708	Effect of potent redox-modulating manganese porphyrin, MnTM-2-PyP, on the Na(+)/H(+) exchangers NHE-1 and NHE-3 in the diabetic rat.
32	20003708	NHE-1 and NHE-3 isoform expression, Na(+),K(+)-ATPase activity, and markers of ROS/RNS-induced damage were determined in kidney homogenates.
33	20003708	Diabetes caused lipid peroxidation, inactivation of aconitase, and increase of nitrotyrosine, which paralleled an increase in NHE-1 and NHE-3 expression and Na(+),K(+)-ATPase activity.
34	20003708	MnTM-2-PyP treatment had no effect on blood glucose and glycosylated hemoglobin, but suppressed lipid peroxidation and nitrotyrosine, protected aconitase against inactivation, and reversed the induction of NHE-1 and NHE-3 isoforms.
35	20003708	Mn(III) alkylpyridylporphyrins were previously found to inhibit activation of major transcription factors, including SP-1 via scavenging of signaling ROS/RNS.
36	21140140	The effect of glucose on the intracellular pH (pH(i)) recovery rate (dpH(i)/dt) and Na(+)-glucose transporter (SGLT) localization was investigated in HEK-293 cells, a cell line that expresses endogenous NHE1, NHE3, SGLT1, and SGLT2 proteins.
37	21140140	Conversely, the chronic effect of high glucose (25 mM) increased the pH(i) recovery rate (~40%, P < 0.05), without changes in the total levels of NHE1, NHE3, or SGLT1 expression, but increasing the total cellular (~50%, P < 0.05) and the plasma membrane (~100%, P < 0.01) content of SGLT2.
38	21140140	Our results indicate that the effect of chronic treatment with a high glucose concentration is associated with increased NHEs activity and plasma membrane expression of SGLT2 in a protein kinase A-dependent way.
39	21140140	The effect of glucose on the intracellular pH (pH(i)) recovery rate (dpH(i)/dt) and Na(+)-glucose transporter (SGLT) localization was investigated in HEK-293 cells, a cell line that expresses endogenous NHE1, NHE3, SGLT1, and SGLT2 proteins.
40	21140140	Conversely, the chronic effect of high glucose (25 mM) increased the pH(i) recovery rate (~40%, P < 0.05), without changes in the total levels of NHE1, NHE3, or SGLT1 expression, but increasing the total cellular (~50%, P < 0.05) and the plasma membrane (~100%, P < 0.01) content of SGLT2.
41	21140140	Our results indicate that the effect of chronic treatment with a high glucose concentration is associated with increased NHEs activity and plasma membrane expression of SGLT2 in a protein kinase A-dependent way.
42	22031848	In a rat model of Li-induced NDI, we studied the effect that sildenafil (Sil), a phosphodiesterase 5 (PDE5) inhibitor, has on renal expression of aquaporin-2 (AQP2), urea transporter UT-A1, Na(+)/H(+) exchanger 3 (NHE3), Na(+)-K(+)-2Cl(-) cotransporter (NKCC2), epithelial Na channel (ENaC; α-, β-, and γ-subunits), endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase.
43	22031848	Semiquantitative immunoblotting revealed the following: in Li+Sil rats, AQP2 expression was partially normalized, whereas that of UT-A1, γ-ENaC, and eNOS was completely normalized; and expression of NKCC2 and NHE3 was significantly higher in Li rats than in controls.
44	22031848	We conclude that, in experimental Li-induced NDI, Sil reduces polyuria, increases urinary osmolality, and decreases free water clearance via upregulation of renal AQP2 and UT-A1.
45	23533381	Combined Effects of PPAR γ Agonists and Epidermal Growth Factor Receptor Inhibitors in Human Proximal Tubule Cells.
46	23533381	We aimed to determine whether epidermal growth factor receptor (EGFR) inhibition, in addition to a peroxisome proliferator-activated receptor gamma (PPAR γ ) agonist, prevents high-glucose-induced proximal tubular fibrosis, inflammation, and sodium and water retention in human proximal tubule cells exposed to normal glucose; high glucose; high glucose with the PPAR γ agonist pioglitazone or with the P-EGFR inhibitor, gefitinib; or high glucose with both pioglitazone and gefitinib.
47	23533381	We have shown that high glucose increases AP-1 and NF κ B binding activity, downstream phosphorylation of EGFR and Erk1/2, and fibronectin and collagen IV expression.
48	23533381	Pioglitazone reversed these effects but upregulated NHE3 and AQP1 expression.
49	23533381	Gefitinib inhibited high glucose induced fibronectin and collagen IV, and EGFR and Erk1/2 phosphorylation and reversed pioglitazone-induced increases in NHE3 and AQP1 expression.
50	23533381	Our data suggests that combination of an EGFR inhibitor and a PPAR γ agonist mitigates high-glucose-induced fibrosis and inflammation and reverses the upregulation of transporters and channels involved in sodium and water retention in human proximal tubule cells.
51	23533381	Hence EGFR blockade may hold promise, not only in limiting tubulointerstitial pathology in diabetic nephropathy, but also in limiting the sodium and water retention observed in patients with diabetes and exacerbated by PPAR γ agonists.
52	23533381	Combined Effects of PPAR γ Agonists and Epidermal Growth Factor Receptor Inhibitors in Human Proximal Tubule Cells.
53	23533381	We aimed to determine whether epidermal growth factor receptor (EGFR) inhibition, in addition to a peroxisome proliferator-activated receptor gamma (PPAR γ ) agonist, prevents high-glucose-induced proximal tubular fibrosis, inflammation, and sodium and water retention in human proximal tubule cells exposed to normal glucose; high glucose; high glucose with the PPAR γ agonist pioglitazone or with the P-EGFR inhibitor, gefitinib; or high glucose with both pioglitazone and gefitinib.
54	23533381	We have shown that high glucose increases AP-1 and NF κ B binding activity, downstream phosphorylation of EGFR and Erk1/2, and fibronectin and collagen IV expression.
55	23533381	Pioglitazone reversed these effects but upregulated NHE3 and AQP1 expression.
56	23533381	Gefitinib inhibited high glucose induced fibronectin and collagen IV, and EGFR and Erk1/2 phosphorylation and reversed pioglitazone-induced increases in NHE3 and AQP1 expression.
57	23533381	Our data suggests that combination of an EGFR inhibitor and a PPAR γ agonist mitigates high-glucose-induced fibrosis and inflammation and reverses the upregulation of transporters and channels involved in sodium and water retention in human proximal tubule cells.
58	23533381	Hence EGFR blockade may hold promise, not only in limiting tubulointerstitial pathology in diabetic nephropathy, but also in limiting the sodium and water retention observed in patients with diabetes and exacerbated by PPAR γ agonists.
59	23933686	SGK1 is activated by insulin and growth factors via phosphatidylinositol-3-kinase, 3-phosphoinositide dependent-kinase PDK1, and mTOR.
60	23933686	NCC, NKCC, NHE1, NHE3, SGLT1, several amino acid transporters) and many ion channels (e.g.
61	23933686	ENaC, SCN5A, TRPV4-6, Orai1/STIM1, ROMK, KCNE1/KCNQ1, GluR6, CFTR).
62	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).
63	24005472	In contrast, the expression of Na(+)/H(+) exchanger-3 (NHE3) and NKCC2 was unchanged in either mouse strain.