The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Pendrin, the Protein Encoded by the Pendred Syndrome Gene (PDS), Is an Apical Porter of Iodide in the Thyroid and Is Regulated by Thyroglobulin in FRTL-5 Cells
Abstract
Pendred syndrome is an autosomal recessive disorder characterized by congenital deafness and thyroid goiter. The thyroid disease typically develops around puberty and is associated with a mild organification defect, characterized by an inappropriate discharge of iodide upon perchlorate stimulation (a positive perchlorate discharge test). The gene (PDS) mutated in Pendred syndrome is expressed in thyroid and encodes a 780-amino acid protein (pendrin) that has recently been shown to function as an iodide/chloride transporter. We sought to establish the location of pendrin in the thyroid and to examine the regulatory network controlling its synthesis. Using peptide-specific antibodies for immunolocalization studies, pendrin was detected in a limited subset of cells within the thyroid follicles, exclusively at the apical membrane of the follicular epithelium. Interestingly, significantly greater amounts of pendrin were encountered in thyroid tissue from patients with Graves' disease. Using a cultured rat thyroid cell line (FRTL-5), PDS expression was found to be significantly induced by low concentrations of thyroglobulin (TG), but not by TSH, sodium iodide, or insulin. This is different from the established effect of TG, more typically a potent suppressor of thyroid-specific gene expression. Together, these results suggest that pendrin is an apical porter of iodide in the thyroid and that the expression and function of both the apical and basal iodide porters are coordinately regulated by follicular TG.
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Cites
Shi, S. R., Key, M. E., & Kalra, K. L. (1991) · Journal of Histochemistry & Cytochemistry · doi:10.1177/39.6.1709656 · Cited by 2,552
Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS)
Everett, L. A., Glaser, B., Beck, J. C., Idol, J. R., Buchs, A., Heyman, M., Adawi, F., Hazani, E., Nassir, E., Baxevanis, A. D., et al. (1997) · Nature Genetics · doi:10.1038/ng1297-411 · Cited by 1,144
Cloning and characterization of the thyroid iodide transporter
Dai, G., Levy, O., & Carrasco, N. (1996) · Nature · doi:10.1038/379458a0 · Cited by 1,109
Hästbacka, J., de la Chapelle, A., Mahtani, M. M., Clines, G., Reeve-Daly, M. P., Daly, M., Hamilton, B. A., Kusumi, K., Trivedi, B., Weaver, A., et al. (1994) · Cell · doi:10.1016/0092-8674(94)90281-x · Cited by 744
The Pendred syndrome gene encodes a chloride-iodide transport protein
Scott, D. A., Wang, R., Kreman, T. M., Sheffield, V. C., & Karniski, L. P. (1999) · Nature Genetics · doi:10.1038/7783 · Cited by 567
Mutations of the Down–regulated in adenoma (DRA) gene cause congenital chloride diarrhoea
Höglund, P., Haila, S., Socha, J., Tomaszewski, L., Saarialho-Kere, U., Karjalainen-Lindsberg, M.-L., Airola, K., Holmberg, C., de la Chapelle, A., & Kere, J. (1996) · Nature Genetics · doi:10.1038/ng1196-316 · Cited by 423
Iodide transport in the thyroid gland
Carrasco, N. (1993) · Biochimica et Biophysica Acta (BBA) - Reviews on Biomembranes · doi:10.1016/0304-4157(93)90017-i · Cited by 365
Iodide Transport in a Continuous Line of Cultured Cells from Rat Thyroid
WEISS, S. J., PHILP, N. J., & GROLLMAN, E. F. (1984) · Endocrinology · doi:10.1210/endo-114-4-1090 · Cited by 337
Pendred, V. (1896) · The Lancet · doi:10.1016/s0140-6736(01)74403-0 · Cited by 310
Everett, L. A., Morsli, H., Wu, D. K., & Green, E. D. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.17.9727 · Cited by 306
Cited by
Sulfonation and molecular action
Strott, C. A. (2002) · Endocrine Reviews · doi:10.1210/er.2001-0040 · Cited by 487
Genetics of congenital hypothyroidism
Park, S. M., & Chatterjee, V. K. K. (2005) · Journal of Medical Genetics · doi:10.1136/jmg.2004.024158 · Cited by 403
Thyroid hormone biosynthesis and release
Carvalho, D. P., & Dupuy, C. (2017) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2017.01.038 · Cited by 346
Genetic disorders coupled to ROS deficiency
O’Neill, S., Brault, J., Stasia, M.-J., & Knaus, U. G. (2015) · Redox Biology · doi:10.1016/j.redox.2015.07.009 · Cited by 164
Functional Characterization of Pendrin in a Polarized Cell System
Gillam, M. P., Sidhaye, A. R., Lee, E. J., Rutishauser, J., Stephan, C. W., & Kopp, P. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m313648200 · Cited by 149
Metadata
- Authors
- Royaux, I. E.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2000-02-01
- Volume
- 141
- Issue
- 2
- Pages
- 839-845
- ISSN
- 0013-7227 (ISSN-L)
- OpenAlex
- W2142844580
- Cited by
- 406
- References
- 30
- FWCI
- 18.38
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Pendrin, the Protein Encoded by the Pendred Syndrome Gene (PDS), Is an Apical Porter of Iodide in the Thyroid and Is Regulated by Thyroglobulin in FRTL-5 Cells. https://app.cochat.ai/papers/10.1210/en.141.2.839
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- Royaux, I. E. (2000). Pendrin, the Protein Encoded by the Pendred Syndrome Gene (PDS), Is an Apical Porter of Iodide in the Thyroid and Is Regulated by Thyroglobulin in FRTL-5 Cells. Endocrinology. https://doi.org/10.1210/en.141.2.839
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