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Sodium–hydrogen antiporter 3

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(Redirected from NHE3)

SLC9A3
Identifiers
AliasesSLC9A3, NHE3, NHE-3, Sodium–hydrogen antiporter 3, DIAR8, solute carrier family 9 member A3
External IDsOMIM: 182307; MGI: 105064; HomoloGene: 55804; GeneCards: SLC9A3; OMA:SLC9A3 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001284351
NM_004174

NM_001081060

RefSeq (protein)

NP_001271280
NP_004165

NP_001074529

Location (UCSC)Chr 5: 0.47 – 0.52 MbChr 13: 74.27 – 74.32 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Sodium–hydrogen antiporter 3 also known as sodium–hydrogen exchanger 3 (NHE3) or solute carrier family 9 member 3 (SLC9A3) is a protein that in humans is encoded by the SLC9A3 gene.[5][6]

SLC9A3 is a sodium–hydrogen antiporter. It is found on the apical side of the epithelial cells of the proximal tubule of the nephron of the kidney, in the apical membrane of enterocytes of the intestine, as well as the basolateral side of both duodenal and pancreatic cells responsible for the release of bicarbonate into the duodenal lumen. It is primarily responsible for maintaining the balance of sodium. It is also indirectly linked to buffering of blood pH. The NHE3 antiporter imports one sodium ion into the cytosol of a tubule cell as it ejects one hydrogen ion from the cell into the lumen of the proximal tubule. The sodium within the tubule cell may then be retained by the body rather than excreted in the urine. The NHE3 antiporter indirectly contributes to blood buffering capacity because hydrogen ions that are ejected are the products of the carbonic anhydrase enzyme, which also makes bicarbonate.[7]

Regulation

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Protein kinase C stimulates NHE3, while protein kinase A inhibits it.[8]

There is a specific protein functioning as an NHE3 regulator, Sodium-hydrogen antiporter 3 regulator 1.

Inhibitors

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Stimulators

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  • Insulin[10] stimulates NHE3 and thereby proximal tubule sodium absorption.

Interactions

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Sodium–hydrogen antiporter 3 has been shown to interact with CHP.[11]

References

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  1. ^ a b c ENSG00000066230 GRCh38: Ensembl release 89: ENSG00000281861, ENSG00000066230Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000036123Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ "Entrez Gene: SLC9A3 Solute carrier family 9 (sodium/hydrogen exchanger), member 3".
  6. ^ Brant SR, Bernstein M, Wasmuth JJ, Taylor EW, McPherson JD, Li X, Walker S, Pouyssegur J, Donowitz M, Tse CM (March 1993). "Physical and genetic mapping of a human apical epithelial Na+/H+ exchanger (NHE3) isoform to chromosome 5p15.3". Genomics. 15 (3): 668–72. doi:10.1006/geno.1993.1122. PMID 8096830.
  7. ^ VI. Mechanisms of Salt & Water Reabsorption Archived February 10, 2007, at the Wayback Machine
  8. ^ 852 Walter F., PhD. Boron (2005). Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 852
  9. ^ Spencer AG, Labonte ED, Rosenbaum DP, Plato CF, Carreras CW, Leadbetter MR, Kozuka K, Kohler J, Koo-McCoy S, He L, Bell N, Tabora J, Joly KM, Navre M, Jacobs JW, Charmot D (2014). "Intestinal inhibition of the Na+/H+ exchanger 3 prevents cardiorenal damage in rats and inhibits Na+ uptake in humans". Sci Transl Med. 6 (227): 227ra36. doi:10.1126/scitranslmed.3007790. PMID 24622516. S2CID 10741924.
  10. ^ Klisic J, Hu MC, Nief V, Reyes L, Fuster D, Moe OW, Ambühl PM (2002). "Insulin activates Na(+)/H(+) exchanger 3: biphasic response and glucocorticoid dependence". Am J Physiol Renal Physiol. 283 (3): F532-9. doi:10.1152/ajprenal.00365.2001. PMID 12167605.
  11. ^ Inoue H, Nakamura Y, Nagita M, Takai T, Masuda M, Nakamura N, Kanazawa H (2003). "Calcineurin homologous protein isoform 2 (CHP2), Na+/H+ exchangers-binding protein, is expressed in intestinal epithelium". Biol. Pharm. Bull. 26 (2): 148–55. doi:10.1248/bpb.26.148. PMID 12576672.

Further reading

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