La pendrine intervient également dans les cellules de la thyroïde, où elle est présente au pôle apical en contact avec le follicule thyroïdien, qui contient la colloïde. Sa fonction est de permettre aux ions iodure I− de franchir la membrane apicale des cellules folliculaire en direction de la colloïde, où ils sont oxydés en diiodeI2 par la thyroperoxydase: cette fonction est indispensable à la biosynthèse des hormones thyroïdiennes.
(en) Susan M. Wall, «The Renal Physiology of Pendrin (SLC26A4) and Its Role in Hypertension», Epithelial Anion Transport in Health and Disease: The Role of the SLC26 Transporters Family: Novartis Foundation Symposium 273, (lire en ligne)DOI10.1002/0470029579.ch15
(en) Lorraine A. Everett, Benjamin Glaser, John C. Beck, Jacquelyn R. Idol, Andreas Buchs, Ma'ayan Heyman, Faiad Adawi, Elizur Hazani, Elias Nassir, Andreas D. Baxevanis, Val C. Sheffield et Eric D. Green, «Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS)», Nature Genetics, vol.17, , p.411-422 (lire en ligne)DOI10.1038/ng1297-411PMID9398842
(en) Markovich D, «Physiological roles and regulation of mammalian sulfate transporters», Physiol. Rev., vol.81, no4, , p.1499–533PMID11581495
(en) Baldwin CT, Weiss S, Farrer LA et al., «Linkage of congenital, recessive deafness (DFNB4) to chromosome 7q31 and evidence for genetic heterogeneity in the Middle Eastern Druze population», Hum. Mol. Genet., vol.4, no9, , p.1637–42DOI10.1093/hmg/4.9.1637PMID8541853
(en) Coyle B, Coffey R, Armour JA et al., «Pendred syndrome (goitre and sensorineural hearing loss) maps to chromosome 7 in the region containing the nonsyndromic deafness gene DFNB4», Nat. Genet., vol.12, no4, , p.421–3DOI10.1038/ng0496-421PMID8630497
(en) Sheffield VC, Kraiem Z, Beck JC et al., «Pendred syndrome maps to chromosome 7q21-34 and is caused by an intrinsic defect in thyroid iodine organification», Nat. Genet., vol.12, no4, , p.424–6DOI10.1038/ng0496-424PMID8630498
(en) Gausden E, Armour JA, Coyle B et al., «Thyroid peroxidase: evidence for disease gene exclusion in Pendred's syndrome», Clin. Endocrinol. (Oxf), vol.44, no4, , p.441–6DOI10.1046/j.1365-2265.1996.714536.xPMID8706311
(en) Coucke P, Van Camp G, Demirhan O et al., «The gene for Pendred syndrome is located between D7S501 and D7S692 in a 1.7-cM region on chromosome 7q», Genomics, vol.40, no1, , p.48–54DOI10.1006/geno.1996.4541PMID9070918
(en) Li XC, Everett LA, Lalwani AK et al., «A mutation in PDS causes non-syndromic recessive deafness», Nat. Genet., vol.18, no3, , p.215–7DOI10.1038/ng0398-215PMID9500541
(en) Van Hauwe P, Everett LA, Coucke P et al., «Two frequent missense mutations in Pendred syndrome», Hum. Mol. Genet., vol.7, no7, , p.1099–104DOI10.1093/hmg/7.7.1099PMID9618166
(en) Coyle B, Reardon W, Herbrick JA et al., «Molecular analysis of the PDS gene in Pendred syndrome», Hum. Mol. Genet., vol.7, no7, , p.1105–12DOI10.1093/hmg/7.7.1105PMID9618167
(en) Usami S, Abe S, Weston MD et al., «Non-syndromic hearing loss associated with enlarged vestibular aqueduct is caused by PDS mutations», Hum. Genet., vol.104, no2, , p.188–92DOI10.1007/s004390050933PMID10190331
(en) Scott DA, Wang R, Kreman TM et al., «The Pendred syndrome gene encodes a chloride-iodide transport protein», Nat. Genet., vol.21, no4, , p.440–3DOI10.1038/7783PMID10192399
(en) Reardon W, OMahoney CF, Trembath R et al., «Enlarged vestibular aqueduct: a radiological marker of pendred syndrome, and mutation of the PDS gene», QJM, vol.93, no2, , p.99–104 (lire en ligne)PMID10700480
(en) Bogazzi F, Raggi F, Ultimieri F et al., «A novel mutation in the pendrin gene associated with Pendred's syndrome», Clin. Endocrinol. (Oxf), vol.52, no3, , p.279–85DOI10.1046/j.1365-2265.2000.00930.xPMID10718825
(en) Bidart JM, Mian C, Lazar V et al., «Expression of pendrin and the Pendred syndrome (PDS) gene in human thyroid tissues», J. Clin. Endocrinol. Metab., vol.85, no5, , p.2028–33DOI10.1210/jc.85.5.2028PMID10843192
(en) Adato A, Raskin L, Petit C, Bonne-Tamir B, «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», Eur. J. Hum. Genet., vol.8, no6, , p.437–42DOI10.1038/sj.ejhg.5200489PMID10878664
(en) Lohi H, Kujala M, Kerkelä E et al., «Mapping of five new putative anion transporter genes in human and characterization of SLC26A6, a candidate gene for pancreatic anion exchanger», Genomics, vol.70, no1, , p.102–12DOI10.1006/geno.2000.6355PMID11087667
(en) Royaux IE, Wall SM, Karniski LP et al., «Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion», Proc. Natl. Acad. Sci. U.S.A., vol.98, no7, , p.4221–6 (PMCID31206)DOI10.1073/pnas.071516798PMID11274445
(en) Campbell C, Cucci RA, Prasad S et al., «Pendred syndrome, DFNB4, and PDS/SLC26A4 identification of eight novel mutations and possible genotype-phenotype correlations», Hum. Mutat., vol.17, no5, , p.403–11DOI10.1002/humu.1116PMID11317356