Sodium-iodide symporter: Wikis

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Solute carrier family 5 (sodium iodide symporter), member 5
Identifiers
Symbols SLC5A5; NIS
External IDs OMIM601843 MGI2149330 HomoloGene37311 GeneCards: SLC5A5 Gene
RNA expression pattern
PBB GE SLC5A5 211123 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 6528 114479
Ensembl ENSG00000105641 ENSMUSG00000000792
UniProt Q92911 Q99PN0
RefSeq (mRNA) NM_000453 NM_053248
RefSeq (protein) NP_000444 NP_444478
Location (UCSC) Chr 19:
17.84 - 17.87 Mb
Chr 8:
73.81 - 73.82 Mb
PubMed search [1] [2]

The sodium-iodide symporter (NIS) also known as solute carrier family 5, member 5 (SLC5A5) is an ion pump that actively transports iodide (I-) across the basolateral membrane into thyroid epithelial cells.[1][2][3] The NIS a member of the sodium/solute symporter family.[4]

Contents

Function

Active transport of iodine into the thyroid gland is an important step in the process of iodide organification and the formation of triiodothyronine (T3) and thyroxine (T4).[5] The symporter is stimulated by TSH, thereby increasing iodine uptake and iodination of tyrosine.[6]

Mechanism

The pump symports two sodium ions for every iodide ion. This symporter is driven by low internal sodium concentration in the thyroid epithelial cells, via facilitated diffusion, caused by the sodium/potassium ATPase pump.[4]

Inhibitors

This pump is the target of certain anion based inhibitors such as perchlorate, pertechnetate, and thiocyanate.[7]

See also


References

  1. ^ Dai G, Levy O, Carrasco N (February 1996). "Cloning and characterization of the thyroid iodide transporter". Nature 379 (6564): 458–60. doi:10.1038/379458a0. PMID 8559252. 
  2. ^ "Entrez Gene: SLC5A5 solute carrier family 5 (sodium iodide symporter), member 5". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=6528. 
  3. ^ Smanik PA, Ryu KY, Theil KS, Mazzaferri EL, Jhiang SM (August 1997). "Expression, exon-intron organization, and chromosome mapping of the human sodium iodide symporter". Endocrinology 138 (8): 3555–8. doi:10.1210/en.138.8.3555. PMID 9231811. 
  4. ^ a b Dohán O, De la Vieja A, Paroder V, Riedel C, Artani M, Reed M, Ginter CS, Carrasco N (February 2003). "The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance". Endocr. Rev. 24 (1): 48–77. doi:10.1210/er.2001-0029. PMID 12588808. 
  5. ^ Dohán O, Portulano C, Basquin C, Reyna-Neyra A, Amzel LM, Carrasco N (December 2007). "The Na+/I- symporter (NIS) mediates electroneutral active transport of the environmental pollutant perchlorate". Proc. Natl. Acad. Sci. U.S.A. 104 (51): 20250–5. doi:10.1073/pnas.0707207104. PMID 18077370. 
  6. ^ Porra V, Ferraro-Peyret C, Durand C, Selmi-Ruby S, Giroud H, Berger-Dutrieux N, Decaussin M, Peix JL, Bournaud C, Orgiazzi J, Borson-Chazot F, Dante R, Rousset B (May 2005). "Silencing of the tumor suppressor gene SLC5A8 is associated with BRAF mutations in classical papillary thyroid carcinomas". J. Clin. Endocrinol. Metab. 90 (5): 3028–35. doi:10.1210/jc.2004-1394. PMID 15687339. 
  7. ^ Van Sande J, Massart C, Beauwens R, Schoutens A, Costagliola S, Dumont JE, Wolff J (January 2003). "Anion selectivity by the sodium iodide symporter". Endocrinology 144 (1): 247–52. doi:10.1210/en.2002-220744. PMID 12488351. 

Further reading

  • Fukushima K, Kaneko CR, Fuchs AF (1992). "The neuronal substrate of integration in the oculomotor system". Prog. Neurobiol. 39 (6): 609–39. doi:10.1016/0301-0082(92)90016-8. PMID 1410443. 
  • De La Vieja A, Dohan O, Levy O, Carrasco N (2000). "Molecular analysis of the sodium/iodide symporter: impact on thyroid and extrathyroid pathophysiology". Physiol. Rev. 80 (3): 1083–105. PMID 10893432. 
  • Dohán O, De la Vieja A, Paroder V, et al. (2003). "The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance". Endocr. Rev. 24 (1): 48–77. doi:10.1210/er.2001-0029. PMID 12588808. 
  • Kogai T, Taki K, Brent GA (2007). "Enhancement of sodium/iodide symporter expression in thyroid and breast cancer". Endocr. Relat. Cancer 13 (3): 797–826. doi:10.1677/erc.1.01143. PMID 16954431. 
  • Riesco-Eizaguirre G, Santisteban P (2006). "A perspective view of sodium iodide symporter research and its clinical implications". Eur. J. Endocrinol. 155 (4): 495–512. doi:10.1530/eje.1.02257. PMID 16990649. 
  • Libert F, Passage E, Lefort A, et al. (1991). "Localization of human thyrotropin receptor gene to chromosome region 14q3 by in situ hybridization". Cytogenet. Cell Genet. 54 (1-2): 82–3. doi:10.1159/000132964. PMID 2249482. 
  • Albero R, Cerdan A, Sanchez Franco F (1988). "Congenital hypothyroidism from complete iodide transport defect: long-term evolution with iodide treatment". Postgraduate medical journal 63 (746): 1043–7. doi:10.1136/pgmj.63.746.1043. PMID 3451231. 
  • Couch RM, Dean HJ, Winter JS (1985). "Congenital hypothyroidism caused by defective iodide transport". J. Pediatr. 106 (6): 950–3. doi:10.1016/S0022-3476(85)80249-3. PMID 3998954. 
  • Smanik PA, Liu Q, Furminger TL, et al. (1996). "Cloning of the human sodium lodide symporter". Biochem. Biophys. Res. Commun. 226 (2): 339–45. doi:10.1006/bbrc.1996.1358. PMID 8806637. 
  • Fujiwara H, Tatsumi K, Miki K, et al. (1997). "Congenital hypothyroidism caused by a mutation in the Na+/I- symporter". Nat. Genet. 16 (2): 124–5. doi:10.1038/ng0697-124. PMID 9171822. 
  • Smanik PA, Ryu KY, Theil KS, et al. (1997). "Expression, exon-intron organization, and chromosome mapping of the human sodium iodide symporter". Endocrinology 138 (8): 3555–8. doi:10.1210/en.138.8.3555. PMID 9231811. 
  • Saito T, Endo T, Kawaguchi A, et al. (1997). "Increased expression of the Na+/I- symporter in cultured human thyroid cells exposed to thyrotropin and in Graves' thyroid tissue". J. Clin. Endocrinol. Metab. 82 (10): 3331–6. doi:10.1210/jc.82.10.3331. PMID 9329364. 
  • Pohlenz J, Medeiros-Neto G, Gross JL, et al. (1997). "Hypothyroidism in a Brazilian kindred due to iodide trapping defect caused by a homozygous mutation in the sodium/iodide symporter gene". Biochem. Biophys. Res. Commun. 240 (2): 488–91. doi:10.1006/bbrc.1997.7594. PMID 9388506. 
  • Matsuda A, Kosugi S (1998). "A homozygous missense mutation of the sodium/iodide symporter gene causing iodide transport defect". J. Clin. Endocrinol. Metab. 82 (12): 3966–71. doi:10.1210/jc.82.12.3966. PMID 9398697. 
  • Pohlenz J, Rosenthal IM, Weiss RE, et al. (1998). "Congenital hypothyroidism due to mutations in the sodium/iodide symporter. Identification of a nonsense mutation producing a downstream cryptic 3' splice site". J. Clin. Invest. 101 (5): 1028–35. doi:10.1172/JCI1504. PMID 9486973. 
  • Venkataraman GM, Yatin M, Ain KB (1998). "Cloning of the human sodium-iodide symporter promoter and characterization in a differentiated human thyroid cell line, KAT-50". Thyroid 8 (1): 63–9. doi:10.1089/thy.1998.8.63. PMID 9492156. 
  • Levy O, Ginter CS, De la Vieja A, et al. (1998). "Identification of a structural requirement for thyroid Na+/I- symporter (NIS) function from analysis of a mutation that causes human congenital hypothyroidism". FEBS Lett. 429 (1): 36–40. doi:10.1016/S0014-5793(98)00522-5. PMID 9657379. 
  • Fujiwara H, Tatsumi K, Miki K, et al. (1998). "Recurrent T354P mutation of the Na+/I- symporter in patients with iodide transport defect". J. Clin. Endocrinol. Metab. 83 (8): 2940–3. doi:10.1210/jc.83.8.2940. PMID 9709973. 
  • Kosugi S, Inoue S, Matsuda A, Jhiang SM (1998). "Novel, missense and loss-of-function mutations in the sodium/iodide symporter gene causing iodide transport defect in three Japanese patients". J. Clin. Endocrinol. Metab. 83 (9): 3373–6. doi:10.1210/jc.83.9.3365. PMID 9745458. 

External links

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