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Pendrin
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<h2 id="function">Function</h2> <p>Pendrin is an ion exchanger found in many types of cells in the body. High levels of pendrin expression have been identified in the inner ear and thyroid.<a class="footnote-ref" id="fnref:7" href="#fn:7"><sup>7</sup></a> </p> <h3>Thyroid</h3> <p>In the thyroid, pendrin is expressed by <a href="/facts/Thyroid_follicular_cell/fFWvPdCt">thyroid follicular cells</a>. <a href="/facts/Sodium%2fiodide_cotransporter/djoG6SI9">Na+/I− symporter</a> imports <a href="/facts/Iodide/JyVRGWMX">iodide (I−)</a> into the cell across its basolateral side, and pendrin extrudes the I− across the cell's apical membrane into the <a href="/facts/Thyroid_colloid/bjovTJVu">thyroid colloid</a>.<a class="footnote-ref" id="fnref:8" href="#fn:8"><sup>8</sup></a> </p> <h3>Inner ear</h3> <p>The exact function of pendrin in the inner ear remains unclear; however, pendrin may play a role in acid-base balance as a chloride-bicarbonate exchanger, regulate volume homeostasis through its ability to function as a chloride-formate exchanger<a class="footnote-ref" id="fnref:9" href="#fn:9"><sup>9</sup></a><a class="footnote-ref" id="fnref:10" href="#fn:10"><sup>10</sup></a> or indirectly modulate the calcium concentration of the endolymph.<a class="footnote-ref" id="fnref:11" href="#fn:11"><sup>11</sup></a> Pendrin is also expressed in the kidney, and has been localized to the apical membrane of a population of intercalated cells in the <a href="/facts/Cortical_collecting_duct/MmpNcpLA">cortical collecting duct</a> where it is involved in bicarbonate secretion.<a class="footnote-ref" id="fnref:12" href="#fn:12"><sup>12</sup></a><a class="footnote-ref" id="fnref:13" href="#fn:13"><sup>13</sup></a> </p> <h3>Kidney</h3> <p>Renal <a href="/facts/Beta-intercalated_cell/MmpNcpLA">β-intercalated cells</a> of the late distal tube and collecting duct express pendrin upon their apical membrane, resorbing one Cl<i>−</i> in exchange for secreting a HCO3−, with Cl− subsequently extruded from the cell by a basolateral Cl− channel. <a href="/facts/Beta-intercalated_cell/MmpNcpLA">β-intercalated cells</a> thus utilise pendrin to contribute to acid-base homeostasis by excreting base (HCO3−) into urine. Additionally, <a href="/facts/Beta-intercalated_cell/MmpNcpLA">β-intercalated cells</a> may use pendrin in concert with a Na+/HCO3−/2Cl− antiporter in order to resorb NaCl.<a class="footnote-ref" id="fnref:14" href="#fn:14"><sup>14</sup></a> </p> <h2 id="clinical-significance">Clinical significance</h2> <p>Mutations in this gene are associated with <a href="/facts/Pendred_syndrome/MSHRgoGD">Pendred syndrome</a>, the most common form of syndromic <a href="/facts/Deafness/PT2xcLaX">deafness</a>, an autosomal-recessive disease. Pendred syndrome is characterized by thyroid goiter and enlargement of the vestibular aqueduct resulting in deafness; however, despite being expressed in the kidney, individuals with Pendred syndrome do not show any kidney-related acid-base, or volume abnormalities under basal conditions. This is probably the result of other bicarbonate or chloride transporters in the kidney compensating for any loss of pendrin function. Only under extreme situations of salt depletion or metabolic alkalosis, or with inactivation of the sodium-chloride cotransporter, are fluid and electrolyte disorders manifested in these patients.<a class="footnote-ref" id="fnref:15" href="#fn:15"><sup>15</sup></a> SLC26A4 is highly homologous to the <a href="/facts/SLC26A3/pqqUWJMH">SLC26A3</a> gene; they have similar genomic structures and this gene is located 3' of the SLC26A3 gene. The encoded protein has homology to sulfate transporters.<a class="footnote-ref" id="fnref:16" href="#fn:16"><sup>16</sup></a> </p><p>Another little-understood role of pendrin is in airway hyperreactivity and <a href="/facts/Inflammation/Ura86MIy">inflammation</a>, as during asthma attacks and allergic reactions. Expression of pendrin in the lung increases in response to allergens and high concentrations of <a href="/facts/Interleukin_13/zEaRbEqc">IL-13</a>,<a class="footnote-ref" id="fnref:17" href="#fn:17"><sup>17</sup></a><a class="footnote-ref" id="fnref:18" href="#fn:18"><sup>18</sup></a> and overexpression of pendrin results in airway inflammation, hyperreactivity, and increased mucus production.<a class="footnote-ref" id="fnref:19" href="#fn:19"><sup>19</sup></a><a class="footnote-ref" id="fnref:20" href="#fn:20"><sup>20</sup></a> These symptoms could result from pendrin's effects on ion concentration in the airway surface liquid, possibly causing the liquid to be less hydrated.<a class="footnote-ref" id="fnref:21" href="#fn:21"><sup>21</sup></a> </p> <h2 id="further-reading">Further reading</h2> <ul><li>Markovich D (October 2001). "Physiological roles and regulation of mammalian sulfate transporters". <i>Physiological Reviews</i>. 81 (4): 1499–1533. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1152%2Fphysrev.2001.81.4.1499">10.1152/physrev.2001.81.4.1499</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/11581495">11581495</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:30942862">30942862</a>.</li> <li>Baldwin CT, Weiss S, Farrer LA, De Stefano AL, Adair R, Franklyn B, et al. (September 1995). "Linkage of congenital, recessive deafness (DFNB4) to chromosome 7q31 and evidence for genetic heterogeneity in the Middle Eastern Druze population". <i>Human Molecular Genetics</i>. 4 (9): 1637–1642. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1093%2Fhmg%2F4.9.1637">10.1093/hmg/4.9.1637</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/8541853">8541853</a>.</li> <li>Coyle B, Coffey R, Armour JA, Gausden E, Hochberg Z, Grossman A, et al. (April 1996). "Pendred syndrome (goitre and sensorineural hearing loss) maps to chromosome 7 in the region containing the nonsyndromic deafness gene DFNB4". <i>Nature Genetics</i>. 12 (4): 421–423. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1038%2Fng0496-421">10.1038/ng0496-421</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/8630497">8630497</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:7166946">7166946</a>.</li> <li>Sheffield VC, Kraiem Z, Beck JC, Nishimura D, Stone EM, Salameh M, et al. (April 1996). "Pendred syndrome maps to chromosome 7q21-34 and is caused by an intrinsic defect in thyroid iodine organification". <i>Nature Genetics</i>. 12 (4): 424–426. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1038%2Fng0496-424">10.1038/ng0496-424</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/8630498">8630498</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:25888014">25888014</a>.</li> <li>Gausden E, Armour JA, Coyle B, Coffey R, Hochberg Z, Pembrey M, et al. (April 1996). "Thyroid peroxidase: evidence for disease gene exclusion in Pendred's syndrome". <i>Clinical Endocrinology</i>. 44 (4): 441–446. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1046%2Fj.1365-2265.1996.714536.x">10.1046/j.1365-2265.1996.714536.x</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/8706311">8706311</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:21410631">21410631</a>.</li> <li>Coucke P, Van Camp G, Demirhan O, Kabakkaya Y, Balemans W, Van Hauwe P, et al. (February 1997). "The gene for Pendred syndrome is located between D7S501 and D7S692 in a 1.7-cM region on chromosome 7q". <i>Genomics</i>. 40 (1): 48–54. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1006%2Fgeno.1996.4541">10.1006/geno.1996.4541</a>. <a href="/facts/Hdl_(identifier)/rdebSxmC">hdl</a>:<a href="https://hdl.handle.net/2066%2F25039">2066/25039</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/9070918">9070918</a>.</li> <li>Li XC, Everett LA, Lalwani AK, Desmukh D, Friedman TB, Green ED, et al. (March 1998). <a href="https://zenodo.org/record/1233379">"A mutation in PDS causes non-syndromic recessive deafness"</a>. <i>Nature Genetics</i>. 18 (3): 215–217. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1038%2Fng0398-215">10.1038/ng0398-215</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/9500541">9500541</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:40830620">40830620</a>.</li> <li>Van Hauwe P, Everett LA, Coucke P, Scott DA, Kraft ML, Ris-Stalpers C, et al. (July 1998). <a href="https://doi.org/10.1093%2Fhmg%2F7.7.1099">"Two frequent missense mutations in Pendred syndrome"</a>. <i>Human Molecular Genetics</i>. 7 (7): 1099–1104. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1093%2Fhmg%2F7.7.1099">10.1093/hmg/7.7.1099</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/9618166">9618166</a>.</li> <li>Coyle B, Reardon W, Herbrick JA, Tsui LC, Gausden E, Lee J, et al. (July 1998). <a href="https://doi.org/10.1093%2Fhmg%2F7.7.1105">"Molecular analysis of the PDS gene in Pendred syndrome"</a>. <i>Human Molecular Genetics</i>. 7 (7): 1105–1112. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1093%2Fhmg%2F7.7.1105">10.1093/hmg/7.7.1105</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/9618167">9618167</a>.</li> <li>Usami S, Abe S, Weston MD, Shinkawa H, Van Camp G, Kimberling WJ (February 1999). "Non-syndromic hearing loss associated with enlarged vestibular aqueduct is caused by PDS mutations". <i>Human Genetics</i>. 104 (2): 188–192. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1007%2Fs004390050933">10.1007/s004390050933</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/10190331">10190331</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:3116063">3116063</a>.</li> <li>Masmoudi S, Charfedine I, Hmani M, Grati M, Ghorbel AM, Elgaied-Boulila A, et al. (January 2000). "Pendred syndrome: phenotypic variability in two families carrying the same PDS missense mutation". <i>American Journal of Medical Genetics</i>. 90 (1): 38–44. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1002%2F%28SICI%291096-8628%2820000103%2990%3A1%3C38%3A%3AAID-AJMG8%3E3.0.CO%3B2-R">10.1002/(SICI)1096-8628(20000103)90:1<38::AID-AJMG8>3.0.CO;2-R</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/10602116">10602116</a>.</li> <li>Reardon W, OMahoney CF, Trembath R, Jan H, Phelps PD (February 2000). <a href="https://doi.org/10.1093%2Fqjmed%2F93.2.99">"Enlarged vestibular aqueduct: a radiological marker of pendred syndrome, and mutation of the PDS gene"</a>. <i>QJM</i>. 93 (2): 99–104. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1093%2Fqjmed%2F93.2.99">10.1093/qjmed/93.2.99</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/10700480">10700480</a>.</li> <li>Bogazzi F, Raggi F, Ultimieri F, Campomori A, Cosci C, Berrettini S, et al. (March 2000). "A novel mutation in the pendrin gene associated with Pendred's syndrome". <i>Clinical Endocrinology</i>. 52 (3): 279–285. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1046%2Fj.1365-2265.2000.00930.x">10.1046/j.1365-2265.2000.00930.x</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/10718825">10718825</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:40121366">40121366</a>.</li> <li>Bidart JM, Mian C, Lazar V, Russo D, Filetti S, Caillou B, et al. (May 2000). <a href="https://doi.org/10.1210%2Fjcem.85.5.6519">"Expression of pendrin and the Pendred syndrome (PDS) gene in human thyroid tissues"</a>. <i>The Journal of Clinical Endocrinology and Metabolism</i>. 85 (5): 2028–2033. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1210%2Fjcem.85.5.6519">10.1210/jcem.85.5.6519</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/10843192">10843192</a>.</li> <li>Adato A, Raskin L, Petit C, Bonne-Tamir B (June 2000). <a href="https://doi.org/10.1038%2Fsj.ejhg.5200489">"Deafness heterogeneity in a Druze isolate from the Middle East: novel OTOF and PDS mutations, low prevalence of GJB2 35delG mutation and indication for a new DFNB locus"</a>. <i>European Journal of Human Genetics</i>. 8 (6): 437–442. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1038%2Fsj.ejhg.5200489">10.1038/sj.ejhg.5200489</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/10878664">10878664</a>.</li> <li>Lohi H, Kujala M, Kerkelä E, Saarialho-Kere U, Kestilä M, Kere J (November 2000). "Mapping of five new putative anion transporter genes in human and characterization of SLC26A6, a candidate gene for pancreatic anion exchanger". <i>Genomics</i>. 70 (1): 102–112. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1006%2Fgeno.2000.6355">10.1006/geno.2000.6355</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/11087667">11087667</a>.</li> <li>Campbell C, Cucci RA, Prasad S, Green GE, Edeal JB, Galer CE, et al. (May 2001). "Pendred syndrome, DFNB4, and PDS/SLC26A4 identification of eight novel mutations and possible genotype-phenotype correlations". <i>Human Mutation</i>. 17 (5): 403–411. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1002%2Fhumu.1116">10.1002/humu.1116</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/11317356">11317356</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:36643824">36643824</a>.</li></ul> <h2 id="external-links">External links</h2> <ul><li><a href="https://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=gene&part=pendred">GeneReviews/NCBI/NIH/UW entry on Pendred Syndrome/DFNB4</a></li> <li><a href="http://oto.wustl.edu/thc/innerear/pendrin-text.htm">Description at oto.wustl.edu</a></li> <li><a href="https://meshb.nlm.nih.gov/record/ui?name=SLC26A4+protein%2C+human">SLC26A4+protein,+human</a> at the U.S. National Library of Medicine <a href="/facts/Medical_Subject_Headings/C57g2JuF">Medical Subject Headings</a> (MeSH)</li></ul> <h2 id="references">References</h2> <ol> <li id="fn:1"><p>"Entrez Gene: SLC26A4 solute carrier family 26, member 4". <a href="https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=5172" target="_blank">https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=5172</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></p></li> <li id="fn:2"><p>Everett LA, Glaser B, Beck JC, Idol JR, Buchs A, Heyman M, et al. (December 1997). "Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS)". Nature Genetics. 17 (4): 411–422. doi:10.1038/ng1297-411. PMID 9398842. S2CID 39359838. <a href="https://zenodo.org/record/1233411" target="_blank">https://zenodo.org/record/1233411</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></p></li> <li id="fn:3"><p>Scott DA, Wang R, Kreman TM, Sheffield VC, Karniski LP (April 1999). "The Pendred syndrome gene encodes a chloride-iodide transport protein". Nature Genetics. 21 (4): 440–443. doi:10.1038/7783. PMID 10192399. S2CID 23717390. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></p></li> <li id="fn:4"><p>Scott DA, Karniski LP (January 2000). "Human pendrin expressed in Xenopus laevis oocytes mediates chloride/formate exchange". American Journal of Physiology. Cell Physiology. 278 (1): C207 – C211. doi:10.1152/ajpcell.2000.278.1.c207. PMID 10644529. S2CID 18841371. <a href="https://doi.org/10.1152%2Fajpcell.2000.278.1.c207" target="_blank">https://doi.org/10.1152%2Fajpcell.2000.278.1.c207</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></p></li> <li id="fn:5"><p>Soleimani M, Greeley T, Petrovic S, Wang Z, Amlal H, Kopp P, et al. (February 2001). "Pendrin: an apical Cl-/OH-/HCO3- exchanger in the kidney cortex". American Journal of Physiology. Renal Physiology. 280 (2): F356 – F364. doi:10.1152/ajprenal.2001.280.2.f356. PMID 11208611. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></p></li> <li id="fn:6"><p>Patterson C, Runge MS (2006). Principles of molecular medicine. Totowa, NJ: Humana Press. p. 957. ISBN 1-58829-202-9. <a href="1-58829-202-9" target="_blank">1-58829-202-9</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></p></li> <li id="fn:7"><p>Bizhanova A, Kopp P (2011-01-01). "Controversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cells". Cellular Physiology and Biochemistry. 28 (3): 485–490. doi:10.1159/000335103. PMID 22116361. <a href="https://doi.org/10.1159%2F000335103" target="_blank">https://doi.org/10.1159%2F000335103</a> <a href="#fnref:7" class="footnote-back-ref">↩</a></p></li> <li id="fn:8"><p>Kessler J, Obinger C, Eales G (July 2008). "Factors influencing the study of peroxidase-generated iodine species and implications for thyroglobulin synthesis". Thyroid. 18 (7): 769–774. doi:10.1089/thy.2007.0310. PMID 18631006. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:8" class="footnote-back-ref">↩</a></p></li> <li id="fn:9"><p>Karniski LP, Aronson PS (September 1985). "Chloride/formate exchange with formic acid recycling: a mechanism of active chloride transport across epithelial membranes". Proceedings of the National Academy of Sciences of the United States of America. 82 (18): 6362–6365. Bibcode:1985PNAS...82.6362K. doi:10.1073/pnas.82.18.6362. PMC 391054. PMID 3862136. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC391054" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC391054</a> <a href="#fnref:9" class="footnote-back-ref">↩</a></p></li> <li id="fn:10"><p>Kim HM, Wangemann P (November 2010). "Failure of fluid absorption in the endolymphatic sac initiates cochlear enlargement that leads to deafness in mice lacking pendrin expression". PLOS ONE. 5 (11): e14041. Bibcode:2010PLoSO...514041K. doi:10.1371/journal.pone.0014041. PMC 2984494. PMID 21103348. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2984494" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2984494</a> <a href="#fnref:10" class="footnote-back-ref">↩</a></p></li> <li id="fn:11"><p>Wangemann P, Nakaya K, Wu T, Maganti RJ, Itza EM, Sanneman JD, et al. (May 2007). 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