PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31971949-2 2020 Previous studies revealed that Solute Carrier Family 26 Member 4 (SLC26A4) being an essential gene of the multi-faceted transporter family SLC26 facilitates reflexive movement of Iodide into follicular lumen through apical membrane of thyrocyte. Iodides 179-185 solute carrier family 26 member 4 Homo sapiens 31-64 33055303-1 2020 Objective: Iodide transport across thyrocytes constitutes a critical step for thyroid hormone biosynthesis, mediated mainly by the basolateral sodium-iodide-symporter (NIS (SLC5A5)) and the apical anion exchanger pendrin (PDS (SLC26A4)). Iodides 11-17 solute carrier family 26 member 4 Homo sapiens 213-220 33055303-1 2020 Objective: Iodide transport across thyrocytes constitutes a critical step for thyroid hormone biosynthesis, mediated mainly by the basolateral sodium-iodide-symporter (NIS (SLC5A5)) and the apical anion exchanger pendrin (PDS (SLC26A4)). Iodides 11-17 solute carrier family 26 member 4 Homo sapiens 227-234 31971949-2 2020 Previous studies revealed that Solute Carrier Family 26 Member 4 (SLC26A4) being an essential gene of the multi-faceted transporter family SLC26 facilitates reflexive movement of Iodide into follicular lumen through apical membrane of thyrocyte. Iodides 179-185 solute carrier family 26 member 4 Homo sapiens 66-73 31971949-3 2020 SLC26A4 gene encodes Pendred protein, a membrane glycoprotein, highly hydrophobic in nature, present at the apical membrane of thyrocyte functioning as transporter of iodide for thyroid cells. Iodides 167-173 solute carrier family 26 member 4 Homo sapiens 0-7 28648509-5 2017 Pendrin has affinity for chloride, iodide, and bicarbonate, among other anions. Iodides 35-41 solute carrier family 26 member 4 Homo sapiens 0-7 31372509-2 2019 Pendrin, the iodide exporter that transports iodide to thyroid follicles, is responsible for Pendred syndrome, a disorder characterized by congenital hypothyroidism and hearing loss. Iodides 13-19 solute carrier family 26 member 4 Homo sapiens 0-7 31372509-2 2019 Pendrin, the iodide exporter that transports iodide to thyroid follicles, is responsible for Pendred syndrome, a disorder characterized by congenital hypothyroidism and hearing loss. Iodides 45-51 solute carrier family 26 member 4 Homo sapiens 0-7 30744098-1 2019 Pendrin (SLC26A4), a Cl-/anion exchanger, is expressed at high levels in kidney, thyroid, and inner ear epithelia, where it has an essential role in bicarbonate secretion/chloride reabsorption, iodide accumulation, and endolymph ion balance, respectively. Iodides 194-200 solute carrier family 26 member 4 Homo sapiens 0-7 30744098-1 2019 Pendrin (SLC26A4), a Cl-/anion exchanger, is expressed at high levels in kidney, thyroid, and inner ear epithelia, where it has an essential role in bicarbonate secretion/chloride reabsorption, iodide accumulation, and endolymph ion balance, respectively. Iodides 194-200 solute carrier family 26 member 4 Homo sapiens 9-16 30774121-5 2019 When iodide is added to a mixed culture of the two cell types, they enter the donor cells via the SLC26A4 transporter and diffuse to the adjacent acceptor cells via GJs where they quench the YFP fluorescence. Iodides 5-11 solute carrier family 26 member 4 Homo sapiens 98-105 29772533-1 2018 We observed local homology between human pendrin and sodium/iodide symporter (NIS), that was absent in the NIS-homologous sodium/monocarboxylate transporter or apical iodide transporter (AIT) which, however, does not transport iodide. Iodides 60-66 solute carrier family 26 member 4 Homo sapiens 41-48 28648509-8 2017 Functional studies have demonstrated that pendrin can mediate iodide efflux in heterologous cells. Iodides 62-68 solute carrier family 26 member 4 Homo sapiens 42-49 28648509-9 2017 This, together with the thyroid phenotype observed in humans (goiter, impaired iodine organification) suggests that pendrin could be involved in iodide efflux into the lumen, one of the steps required for thyroid hormone synthesis. Iodides 145-151 solute carrier family 26 member 4 Homo sapiens 116-123 26444544-7 2015 When iodide was added, it was transported into donor cells by SLC26A4, diffused through the GJs to acceptor cells, and quenched the YFP(QL) fluorescence. Iodides 5-11 solute carrier family 26 member 4 Homo sapiens 62-69 27161422-4 2016 METHODS: Pendrin activity was evaluated by measuring pendrin-dependent iodide influx following overexpression of the transporter in a human kidney cell line, in the presence of selected test compounds or the respective vehicles. Iodides 71-77 solute carrier family 26 member 4 Homo sapiens 9-16 27161422-4 2016 METHODS: Pendrin activity was evaluated by measuring pendrin-dependent iodide influx following overexpression of the transporter in a human kidney cell line, in the presence of selected test compounds or the respective vehicles. Iodides 71-77 solute carrier family 26 member 4 Homo sapiens 53-60 26313899-9 2015 SUMMARY: Anoctamin and pendrin are two plausible candidates as mediators of apical iodide efflux. Iodides 83-89 solute carrier family 26 member 4 Homo sapiens 23-30 26313899-0 2015 Pendrin and anoctamin as mediators of apical iodide efflux in thyroid cells. Iodides 45-51 solute carrier family 26 member 4 Homo sapiens 0-7 26313899-5 2015 RECENT FINDINGS: The functional characterization of pendrin (PDS/SLC26A4), a multifunctional anion exchanger, suggested that it could be involved in mediating iodide efflux. Iodides 159-165 solute carrier family 26 member 4 Homo sapiens 52-59 26313899-5 2015 RECENT FINDINGS: The functional characterization of pendrin (PDS/SLC26A4), a multifunctional anion exchanger, suggested that it could be involved in mediating iodide efflux. Iodides 159-165 solute carrier family 26 member 4 Homo sapiens 65-72 25960948-4 2013 The presence of two mutant alleles of SLC26A4 is associated with abnormal iodide organification, increased thyroid gland volume, increased severity of hearing loss, and bilateral EVA. Iodides 74-80 solute carrier family 26 member 4 Homo sapiens 38-45 26285906-6 2015 This review covers the three known iodide transporters - the sodium iodide symporter, pendrin and the sodium-coupled monocarboxylate transporter - and their role in iodide transport in breast cells, along with efforts to manipulate them to increase the potential for radioiodide therapy as a treatment for breast cancer. Iodides 35-41 solute carrier family 26 member 4 Homo sapiens 86-93 25960948-5 2013 The presence of a single mutant allele of SLC26A4 is associated with normal iodide organification, normal thyroid gland volume, less severe hearing loss and either bilateral or unilateral EVA. Iodides 76-82 solute carrier family 26 member 4 Homo sapiens 42-49 23322815-1 2013 CONTEXT: Pendrin is a transmembrane protein located at the apical end of the thyrocyte in which it mediates the efflux of iodide through the thyroid follicular cell. Iodides 122-128 solute carrier family 26 member 4 Homo sapiens 9-16 21358184-6 2011 SLC26A4 encodes the pendrin polypeptide, an anion exchanger that, in recombinant expression systems, transports chloride, bicarbonate, and iodide. Iodides 139-145 solute carrier family 26 member 4 Homo sapiens 0-7 21550633-3 2011 Because transport of iodide from the thyroid follicular cells to the follicular lumen is mediated by the protein pendrin at the apical surface, we hypothesized that perchlorate may also interact with this protein. Iodides 21-27 solute carrier family 26 member 4 Homo sapiens 113-120 21550633-8 2011 Thus, recombinant HeLa cells expressing pendrin protein accumulate iodide and perchlorate intracellularly, indicating that pendrin is involved in the uptake of perchlorate. Iodides 67-73 solute carrier family 26 member 4 Homo sapiens 40-47 21550633-8 2011 Thus, recombinant HeLa cells expressing pendrin protein accumulate iodide and perchlorate intracellularly, indicating that pendrin is involved in the uptake of perchlorate. Iodides 67-73 solute carrier family 26 member 4 Homo sapiens 123-130 21550633-9 2011 Additional results from this study suggest that iodide and perchlorate competitively inhibit each other for uptake by pendrin. Iodides 48-54 solute carrier family 26 member 4 Homo sapiens 118-125 21511235-4 2011 In the thyroid, pendrin is expressed at the apical membrane of thyroid follicular cells and it appears to be involved in mediating iodide efflux into the lumen and/or maintenance of the follicular pH. Iodides 131-137 solute carrier family 26 member 4 Homo sapiens 16-23 22109890-4 2012 The discovery of mutations in the SLC26A4 gene in patients with Pendred syndrome (congenital deafness, goiter, and defective iodide organification) suggested a possible role for the encoded protein, pendrin, as an apical iodide transporter. Iodides 125-131 solute carrier family 26 member 4 Homo sapiens 34-41 22109890-4 2012 The discovery of mutations in the SLC26A4 gene in patients with Pendred syndrome (congenital deafness, goiter, and defective iodide organification) suggested a possible role for the encoded protein, pendrin, as an apical iodide transporter. Iodides 125-131 solute carrier family 26 member 4 Homo sapiens 199-206 21551164-1 2011 INTRODUCTION: Pendred syndrome, a combination of sensorineural deafness, impaired organification of iodide in the thyroid and goitre, results from biallelic defects in pendrin (encoded by SLC26A4), which transports chloride and iodide in the inner ear and thyroid respectively. Iodides 100-106 solute carrier family 26 member 4 Homo sapiens 168-175 21551164-1 2011 INTRODUCTION: Pendred syndrome, a combination of sensorineural deafness, impaired organification of iodide in the thyroid and goitre, results from biallelic defects in pendrin (encoded by SLC26A4), which transports chloride and iodide in the inner ear and thyroid respectively. Iodides 228-234 solute carrier family 26 member 4 Homo sapiens 168-175 21551164-1 2011 INTRODUCTION: Pendred syndrome, a combination of sensorineural deafness, impaired organification of iodide in the thyroid and goitre, results from biallelic defects in pendrin (encoded by SLC26A4), which transports chloride and iodide in the inner ear and thyroid respectively. Iodides 228-234 solute carrier family 26 member 4 Homo sapiens 188-195 21358184-6 2011 SLC26A4 encodes the pendrin polypeptide, an anion exchanger that, in recombinant expression systems, transports chloride, bicarbonate, and iodide. Iodides 139-145 solute carrier family 26 member 4 Homo sapiens 20-27 22116353-1 2011 Pendrin (SLC26A4), a Cl(-)/anion exchanger encoded by the gene PDS, is highly expressed in the kidney, thyroid and inner ear epithelia and is essential for bicarbonate secretion/chloride reabsorption, iodide accumulation and endolymph ion balance, respectively. Iodides 201-207 solute carrier family 26 member 4 Homo sapiens 9-16 22116353-1 2011 Pendrin (SLC26A4), a Cl(-)/anion exchanger encoded by the gene PDS, is highly expressed in the kidney, thyroid and inner ear epithelia and is essential for bicarbonate secretion/chloride reabsorption, iodide accumulation and endolymph ion balance, respectively. Iodides 201-207 solute carrier family 26 member 4 Homo sapiens 0-7 22116353-1 2011 Pendrin (SLC26A4), a Cl(-)/anion exchanger encoded by the gene PDS, is highly expressed in the kidney, thyroid and inner ear epithelia and is essential for bicarbonate secretion/chloride reabsorption, iodide accumulation and endolymph ion balance, respectively. Iodides 201-207 solute carrier family 26 member 4 Homo sapiens 63-66 22116356-2 2011 Pendrin (SLC26A4) is inserted into the apical membrane of thyrocytes and thought to be involved in mediating iodide efflux. Iodides 109-115 solute carrier family 26 member 4 Homo sapiens 0-7 22116356-2 2011 Pendrin (SLC26A4) is inserted into the apical membrane of thyrocytes and thought to be involved in mediating iodide efflux. Iodides 109-115 solute carrier family 26 member 4 Homo sapiens 9-16 22116356-3 2011 METHODS: We determined the effects of carboxy-terminal mutations of pendrin on the cellular localization and the ability to transport iodide. Iodides 134-140 solute carrier family 26 member 4 Homo sapiens 68-75 22116356-8 2011 CONCLUSION: Pendrin membrane abundance and its ability to mediate iodide efflux increase after activation of the PKA pathway. Iodides 66-72 solute carrier family 26 member 4 Homo sapiens 12-19 22116358-2 2011 In the thyroid, pendrin is expressed at the apical membrane of the follicular epithelium and may be involved in mediating apical iodide efflux into the follicle; in the inner ear, it plays a crucial role in the conditioning of the pH and ion composition of the endolymph; in the kidney, it may exert a role in pH homeostasis and regulation of blood pressure. Iodides 129-135 solute carrier family 26 member 4 Homo sapiens 16-23 22116359-1 2011 BACKGROUND: Pendrin is a multifunctional anion transporter that exchanges chloride and iodide in the thyroid, as well as chloride and bicarbonate in the inner ear, kidney and airways. Iodides 87-93 solute carrier family 26 member 4 Homo sapiens 12-19 22116360-1 2011 BACKGROUND: Pendrin is a transport protein exchanging chloride for other anions, such as iodide in the thyroid gland or bicarbonate in the inner ear. Iodides 89-95 solute carrier family 26 member 4 Homo sapiens 12-19 22116360-8 2011 RESULTS: Both the Cl(-)/I(-) and the Cl(-)/OH(-) exchange activities of pendrin V239D, G334V X335 and I487Y FSX39 were significantly reduced with respect to the wild type, with V239D displaying a residual iodide transport. Iodides 205-211 solute carrier family 26 member 4 Homo sapiens 72-79 22116361-4 2011 The clinical phenotype of patients with Pendred syndrome and the fact that pendrin can mediate iodide efflux in transfected cells suggest that this anion exchanger may be involved in mediating iodide efflux into the follicular lumen, a key step in thyroid hormone biosynthesis. Iodides 95-101 solute carrier family 26 member 4 Homo sapiens 75-82 22116361-4 2011 The clinical phenotype of patients with Pendred syndrome and the fact that pendrin can mediate iodide efflux in transfected cells suggest that this anion exchanger may be involved in mediating iodide efflux into the follicular lumen, a key step in thyroid hormone biosynthesis. Iodides 193-199 solute carrier family 26 member 4 Homo sapiens 75-82 22116361-6 2011 This review discusses supporting evidence as well as arguments questioning a role of pendrin in mediating iodide efflux in thyrocytes. Iodides 106-112 solute carrier family 26 member 4 Homo sapiens 85-92 22116362-8 2011 Moreover, ectopic expression of pendrin in transfected non-thyroid cells is capable of mediating iodide efflux. Iodides 97-103 solute carrier family 26 member 4 Homo sapiens 32-39 22116362-9 2011 It is concluded that pendrin may participate in the iodide efflux into thyroid lumen but not as the unique transporter. Iodides 52-58 solute carrier family 26 member 4 Homo sapiens 21-28 30780803-5 2010 Pendrin is the primary protein that is responsible for iodide efflux out of the thyrocyte and into the follicular lumen. Iodides 55-61 solute carrier family 26 member 4 Homo sapiens 0-7 20298745-5 2010 In the thyroid, pendrin localizes to the apical membrane of thyrocytes, where it may be involved in mediating iodide efflux. Iodides 110-116 solute carrier family 26 member 4 Homo sapiens 16-23 20298745-6 2010 Loss-of-function mutations in the SLC26A4 gene are associated with a partial iodide organification defect, presumably because of a reduced iodide efflux into the follicular lumen. Iodides 77-83 solute carrier family 26 member 4 Homo sapiens 34-41 18692402-3 2008 Pendred syndrome is caused by biallelic mutations in the SLC26A4 gene, which encodes pendrin, a transporter of chloride, bicarbonate and iodide. Iodides 137-143 solute carrier family 26 member 4 Homo sapiens 85-92 30290408-3 2008 SLC26A4 encodes pendrin, a sodium-independent transporter of iodide/chloride, chloride/formate and bicarbonate, that is expressed in the inner ear, thyroid gland, syncytiotrophoblast cells, endometrium and kidney. Iodides 61-67 solute carrier family 26 member 4 Homo sapiens 0-7 30290408-3 2008 SLC26A4 encodes pendrin, a sodium-independent transporter of iodide/chloride, chloride/formate and bicarbonate, that is expressed in the inner ear, thyroid gland, syncytiotrophoblast cells, endometrium and kidney. Iodides 61-67 solute carrier family 26 member 4 Homo sapiens 16-23 19429184-2 2009 The SLC26A4 gene is expressed at the apical surface of thyrocytes and its product forms an efficient iodide-trapping mechanism. Iodides 101-107 solute carrier family 26 member 4 Homo sapiens 4-11 19196800-9 2009 Biallelic mutations in the SLC26A4 gene lead to Pendred syndrome, an autosomal recessive disorder characterized by sensorineural deafness, goiter, and impaired iodide organification. Iodides 160-166 solute carrier family 26 member 4 Homo sapiens 27-34 19196800-11 2009 Functional in vitro data and the impaired iodide organification observed in patients with Pendred syndrome support a role of pendrin as an apical iodide transporter. Iodides 42-48 solute carrier family 26 member 4 Homo sapiens 125-132 19050049-1 2009 CONTEXT: Pendrin is an apical protein of thyroid follicular cells, responsible for the efflux of iodide into the follicular lumen via an iodide-chloride transport mechanism. Iodides 97-103 solute carrier family 26 member 4 Homo sapiens 9-16 19050049-1 2009 CONTEXT: Pendrin is an apical protein of thyroid follicular cells, responsible for the efflux of iodide into the follicular lumen via an iodide-chloride transport mechanism. Iodides 137-143 solute carrier family 26 member 4 Homo sapiens 9-16 18692402-3 2008 Pendred syndrome is caused by biallelic mutations in the SLC26A4 gene, which encodes pendrin, a transporter of chloride, bicarbonate and iodide. Iodides 137-143 solute carrier family 26 member 4 Homo sapiens 57-64 18692402-4 2008 This review discusses the controversies surrounding the potential role of pendrin in mediating apical iodide efflux into the lumen of thyroid follicles, and discusses its functional role in the kidney and the inner ear. Iodides 102-108 solute carrier family 26 member 4 Homo sapiens 74-81 16684826-12 2006 The mutant pendrin (p.R776C) retained its ability to transport iodide in vitro. Iodides 63-69 solute carrier family 26 member 4 Homo sapiens 11-18 18322141-1 2008 Pendrin, a Cl(-)/anion exchanger encoded by the gene PDS, is highly expressed in the kidney, thyroid, and inner ear epithelia and is essential for bicarbonate secretion, iodide accumulation, and endolymph ion balance, respectively. Iodides 170-176 solute carrier family 26 member 4 Homo sapiens 0-7 18322141-1 2008 Pendrin, a Cl(-)/anion exchanger encoded by the gene PDS, is highly expressed in the kidney, thyroid, and inner ear epithelia and is essential for bicarbonate secretion, iodide accumulation, and endolymph ion balance, respectively. Iodides 170-176 solute carrier family 26 member 4 Homo sapiens 53-56 18538122-2 2008 The Pendred syndrome gene (SLC26A4) encodes a new anion exchanger named pendrin which mediates iodide transport by thyrocytes and regulates ion and fluid transport by the endolymphatic sac epithelium. Iodides 95-101 solute carrier family 26 member 4 Homo sapiens 27-34 18538122-2 2008 The Pendred syndrome gene (SLC26A4) encodes a new anion exchanger named pendrin which mediates iodide transport by thyrocytes and regulates ion and fluid transport by the endolymphatic sac epithelium. Iodides 95-101 solute carrier family 26 member 4 Homo sapiens 72-79 16648292-4 2006 In addition, we found that PDS gene was induced by TSH/cAMP and iodide in the presence of Tg. Iodides 64-70 solute carrier family 26 member 4 Homo sapiens 27-30 16924389-4 2006 Expression of the SLC26A4 gene may be responsible for iodide transport in the thyroid as well as for formation and function of the inner ear. Iodides 54-60 solute carrier family 26 member 4 Homo sapiens 18-25 16791000-2 2006 It is assumed that SLC26A4 acts as a chloride/anion exchanger responsible for the iodide organification in the thyroid gland, and conditioning of the endolymphatic fluid in the inner ear. Iodides 82-88 solute carrier family 26 member 4 Homo sapiens 19-26 16791000-6 2006 Furthermore, we show that the SLC26A4 induced chloride uptake in HEK293-Phoenix cells competes with iodide, and, in addition, that the chloride uptake can be blocked by NPPB and niflumic acid, whereas DIDS is ineffective. Iodides 100-106 solute carrier family 26 member 4 Homo sapiens 30-37 16914891-2 2006 It is generally assumed that SLC26A4 acts as a chloride/anion exchanger, which in the thyroid gland transports iodide, and in the inner ear contributes to the conditioning of the endolymphatic fluid. Iodides 111-117 solute carrier family 26 member 4 Homo sapiens 29-36 16914891-4 2006 The validation of the method was done by functionally characterizing the chloride/iodide transport of SLC26A4, and a mutant, i.e. SLC26A4(S28R), which we previously described in a patient with sensorineural hearing loss, hypothyroidism and goiter. Iodides 82-88 solute carrier family 26 member 4 Homo sapiens 102-109 16914891-5 2006 Using the fluorometric method we describe here we can continuously monitor and quantify the iodide or chloride amounts transported by the cells, and we found that the transport capability of the SLC26A4(S28R) mutant protein is markedly reduced if compared to wild-type SLC26A4. Iodides 92-98 solute carrier family 26 member 4 Homo sapiens 195-202 16260428-1 2005 OBJECTIVE: The SLC26A4 protein (pendrin) seems to be involved in the exchange of chloride with other anions, therefore being responsible for iodide organification in the thyroid gland and the conditioning of the endolymphatic fluid in the inner ear. Iodides 141-147 solute carrier family 26 member 4 Homo sapiens 15-22 16260428-1 2005 OBJECTIVE: The SLC26A4 protein (pendrin) seems to be involved in the exchange of chloride with other anions, therefore being responsible for iodide organification in the thyroid gland and the conditioning of the endolymphatic fluid in the inner ear. Iodides 141-147 solute carrier family 26 member 4 Homo sapiens 32-39 15001644-1 2004 Iodide transport by thyrocytes involves two transporters, namely the Na(+)/I (-) symporter located at the basolateral pole and possibly pendrin in the apical membranes of the cell. Iodides 0-6 solute carrier family 26 member 4 Homo sapiens 136-143 15942636-1 2005 The Pendred syndrome gene (PDS) encodes a transmembrane protein, pendrin, which is expressed in follicular thyroid cells and participates in the apical iodide transport. Iodides 152-158 solute carrier family 26 member 4 Homo sapiens 65-72 16053392-11 2005 In functional studies, these mutants lose the ability of pendrin to mediate iodide efflux. Iodides 76-82 solute carrier family 26 member 4 Homo sapiens 57-64 14715652-13 2004 These results provide evidence that pendrin mediates apical iodide efflux from polarized mammalian cells loaded with iodide. Iodides 60-66 solute carrier family 26 member 4 Homo sapiens 36-43 14715652-13 2004 These results provide evidence that pendrin mediates apical iodide efflux from polarized mammalian cells loaded with iodide. Iodides 117-123 solute carrier family 26 member 4 Homo sapiens 36-43 14715652-14 2004 Consistent with the partial organification defect observed in patients with Pendred"s syndrome, naturally occurring mutations of pendrin lead to impaired transport of iodide. Iodides 167-173 solute carrier family 26 member 4 Homo sapiens 129-136 14530519-0 2003 Pendrin transporter carries out iodide uptake into MCF-7 human mammary cancer cells. Iodides 32-38 solute carrier family 26 member 4 Homo sapiens 0-7 12107249-0 2002 Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells. Iodides 14-20 solute carrier family 26 member 4 Homo sapiens 0-7 12533525-8 2003 These results suggest that pendrin may play a role in thyroid hormone production as the apical porter of chloride/iodide and investigation of pendrin leads to a better understanding of functional aspects of the iodine transportation system in thyroid diseases. Iodides 114-120 solute carrier family 26 member 4 Homo sapiens 27-34 12727986-4 2003 Pendrin is an apical porter of iodide in the thyroid. Iodides 31-37 solute carrier family 26 member 4 Homo sapiens 0-7 12354788-2 2002 Mutations in the transmembrane protein, pendrin, cause diminished export of iodide from thyroid follicular cells to the colloid and are associated with the syndrome. Iodides 76-82 solute carrier family 26 member 4 Homo sapiens 40-47 12107249-0 2002 Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells. Iodides 60-66 solute carrier family 26 member 4 Homo sapiens 0-7 11932316-4 2002 PDS is thought to enable efflux iodide into the follicle lumen. Iodides 32-38 solute carrier family 26 member 4 Homo sapiens 0-3 11932304-3 2002 It has been postulated that in the thyroid pendrin could participate in the transport of iodide from the cell to the lumen of follicles. Iodides 89-95 solute carrier family 26 member 4 Homo sapiens 43-50 11932316-9 2002 Iodide efflux assays were performed using human embryonic kidney 293 cells transfected with mutant pendrin and cotransfected with sodium iodide transporter to provide a mechanism of iodide uptake. Iodides 0-6 solute carrier family 26 member 4 Homo sapiens 99-106 11573132-4 2001 A candidate for the apical iodide-permeating mechanism is pendrin, a chloride/iodide transporting protein recently identified in the apical membrane. Iodides 27-33 solute carrier family 26 member 4 Homo sapiens 58-65 11919333-2 2002 It codes for a transmembrane protein called pendrin, which is highly expressed at the apical surface of the thyroid cell and functions as a transporter of chloride and iodide. Iodides 168-174 solute carrier family 26 member 4 Homo sapiens 44-51 11836344-1 2002 Expression of the Pendred syndrome gene (PDS/Pds) is thought to be responsible for the iodide transport in the thyroid as well as the formation and function of the inner ear. Iodides 87-93 solute carrier family 26 member 4 Homo sapiens 41-44 11836344-1 2002 Expression of the Pendred syndrome gene (PDS/Pds) is thought to be responsible for the iodide transport in the thyroid as well as the formation and function of the inner ear. Iodides 87-93 solute carrier family 26 member 4 Homo sapiens 45-48 11248751-1 2001 OBJECTIVE: The expression of two recently identified iodide transporters, namely the sodium/iodide symporter (NIS) and pendrin, the product of the gene responsible for the Pendred syndrome (PDS), was studied in a series of various extra-thyroidal human tissues, and especially in those known to concentrate iodide. Iodides 53-59 solute carrier family 26 member 4 Homo sapiens 119-126 11248751-1 2001 OBJECTIVE: The expression of two recently identified iodide transporters, namely the sodium/iodide symporter (NIS) and pendrin, the product of the gene responsible for the Pendred syndrome (PDS), was studied in a series of various extra-thyroidal human tissues, and especially in those known to concentrate iodide. Iodides 53-59 solute carrier family 26 member 4 Homo sapiens 190-193 11573133-0 2001 The role of pendrin in iodide regulation. Iodides 23-29 solute carrier family 26 member 4 Homo sapiens 12-19 11573133-4 2001 Despite its high homology to known sulfate transporters, pendrin has been shown to transport iodide and chloride, but not sulfate. Iodides 93-99 solute carrier family 26 member 4 Homo sapiens 57-64 10843192-2 2000 Its product, designated pendrin, was shown to transport chloride and iodide. Iodides 69-75 solute carrier family 26 member 4 Homo sapiens 24-31 11137035-0 2001 Effects of thyroglobulin and pendrin on iodide flux through the thyrocyte. Iodides 40-46 solute carrier family 26 member 4 Homo sapiens 29-36 10861298-1 2000 The PDS gene encodes a transmembrane protein, known as pendrin, which functions as a transporter of iodide and chloride. Iodides 100-106 solute carrier family 26 member 4 Homo sapiens 4-7 10861298-1 2000 The PDS gene encodes a transmembrane protein, known as pendrin, which functions as a transporter of iodide and chloride. Iodides 100-106 solute carrier family 26 member 4 Homo sapiens 55-62 10861298-5 2000 The mutations associated with Pendred syndrome have complete loss of pendrin-induced chloride and iodide transport, while alleles unique to people with DFNB4 are able to transport both iodide and chloride, albeit at a much lower level than wild-type pendrin. Iodides 185-191 solute carrier family 26 member 4 Homo sapiens 152-157 10861298-7 2000 We propose a model for pendrin function in the thyroid in which pendrin transports iodide across the apical membrane of the thyrocyte into the colloid space. Iodides 83-89 solute carrier family 26 member 4 Homo sapiens 23-30 10861298-7 2000 We propose a model for pendrin function in the thyroid in which pendrin transports iodide across the apical membrane of the thyrocyte into the colloid space. Iodides 83-89 solute carrier family 26 member 4 Homo sapiens 64-71 10571950-3 1999 The disease gene (PDS) has been mapped to chromosome 7q22-q31, and encodes a chloride-iodide transport protein. Iodides 86-92 solute carrier family 26 member 4 Homo sapiens 18-21 10192399-7 1999 The rates of transport for iodide and chloride were significantly increased following the expression of pendrin in both cell systems. Iodides 27-33 solute carrier family 26 member 4 Homo sapiens 104-111 10192399-8 1999 Our results demonstrate that pendrin functions as a transporter of chloride and iodide, but not sulfate, and may provide insight into thyroid physiology and the pathophysiology of Pendred syndrome. Iodides 80-86 solute carrier family 26 member 4 Homo sapiens 29-36 35227018-9 2022 In the thyroid, CFTR and pendrin might have overlapping functions in driving the apical flux of iodide within the follicular lumen. Iodides 96-102 solute carrier family 26 member 4 Homo sapiens 25-32 35227018-3 2022 While pendrin drives chloride reabsorption and bicarbonate, thiocyanate or iodide secretion within the apical compartment, CFTR represents a pathway for the apical efflux of chloride, bicarbonate, and possibly iodide. Iodides 75-81 solute carrier family 26 member 4 Homo sapiens 6-13