Rujukan Pendrin

↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
1 2 "Entrez Gene: SLC26A4 solute carrier family 26, member 4".
↑ Everett LA, Glaser B, Beck JC, Idol JR, Buchs A, Heyman M, Adawi F, Hazani E, Nassir E, Baxevanis AD, Sheffield VC, Green ED (December 1997). "Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS)". Nature Genetics. 17 (4): 411–22. doi:10.1038/ng1297-411. PMID 9398842. S2CID 39359838.
↑ 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): 440–3. doi:10.1038/7783. PMID 10192399. S2CID 23717390.
↑ 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): C207-11. doi:10.1152/ajpcell.2000.278.1.c207. PMID 10644529. S2CID 18841371.
↑ Soleimani M, Greeley T, Petrovic S, Wang Z, Amlal H, Kopp P, Burnham CE (February 2001). "Pendrin: an apical Cl-/OH-/HCO3- exchanger in the kidney cortex". American Journal of Physiology. Renal Physiology. 280 (2): F356-64. doi:10.1152/ajprenal.2001.280.2.f356. PMID 11208611.
↑ Patterson C, Runge MS (2006). Principles of molecular medicine. Totowa, NJ: Humana Press. m/s. 957. ISBN 1-58829-202-9.
↑ 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): 485–90. doi:10.1159/000335103. PMID 22116361.
↑ 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): 6362–5. Bibcode:1985PNAS...82.6362K. doi:10.1073/pnas.82.18.6362. PMC 391054. PMID 3862136.
↑ 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.
↑ Wangemann P, Nakaya K, Wu T, Maganti RJ, Itza EM, Sanneman JD, Harbidge DG, Billings S, Marcus DC (May 2007). "Loss of cochlear HCO3- secretion causes deafness via endolymphatic acidification and inhibition of Ca2+ reabsorption in a Pendred syndrome mouse model". American Journal of Physiology. Renal Physiology. 292 (5): F1345-53. doi:10.1152/ajprenal.00487.2006. PMC 2020516. PMID 17299139.
↑ Wall SM (2006). "The renal physiology of pendrin (SLC26A4) and its role in hypertension". Novartis Foundation Symposium. Novartis Foundation Symposia. 273: 231–9, discussion 239–43, 261–4. doi:10.1002/0470029579.ch15. ISBN 978-0-470-02957-2. PMID 17120771.
↑ Royaux IE, Wall SM, Karniski LP, Everett LA, Suzuki K, Knepper MA, Green ED (March 2001). "Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion". Proceedings of the National Academy of Sciences of the United States of America. 98 (7): 4221–6. Bibcode:2001PNAS...98.4221R. doi:10.1073/pnas.071516798. PMC 31206. PMID 11274445.
↑ Pela I, Bigozzi M, Bianchi B (June 2008). "Profound hypokalemia and hypochloremic metabolic alkalosis during thiazide therapy in a child with Pendred syndrome". Clinical Nephrology. 69 (6): 450–3. doi:10.5414/cnp69450. PMID 18538122.
↑ Kuperman DA, Lewis CC, Woodruff PG, Rodriguez MW, Yang YH, Dolganov GM, Fahy JV, Erle DJ (August 2005). "Dissecting asthma using focused transgenic modeling and functional genomics". The Journal of Allergy and Clinical Immunology. 116 (2): 305–11. doi:10.1016/j.jaci.2005.03.024. PMID 16083784.
↑ Zhen G, Park SW, Nguyenvu LT, Rodriguez MW, Barbeau R, Paquet AC, Erle DJ (February 2007). "IL-13 and epidermal growth factor receptor have critical but distinct roles in epithelial cell mucin production". American Journal of Respiratory Cell and Molecular Biology. 36 (2): 244–53. doi:10.1165/rcmb.2006-0180OC. PMC 1899314. PMID 16980555.
↑ Pedemonte N, Caci E, Sondo E, Caputo A, Rhoden K, Pfeffer U, Di Candia M, Bandettini R, Ravazzolo R, Zegarra-Moran O, Galietta LJ (April 2007). "Thiocyanate transport in resting and IL-4-stimulated human bronchial epithelial cells: role of pendrin and anion channels". Journal of Immunology. 178 (8): 5144–53. doi:10.4049/jimmunol.178.8.5144. PMID 17404297.
↑ Nakao I, Kanaji S, Ohta S, Matsushita H, Arima K, Yuyama N, Yamaya M, Nakayama K, Kubo H, Watanabe M, Sagara H, Sugiyama K, Tanaka H, Toda S, Hayashi H, Inoue H, Hoshino T, Shiraki A, Inoue M, Suzuki K, Aizawa H, Okinami S, Nagai H, Hasegawa M, Fukuda T, Green ED, Izuhara K (May 2008). "Identification of pendrin as a common mediator for mucus production in bronchial asthma and chronic obstructive pulmonary disease". Journal of Immunology. 180 (9): 6262–9. doi:10.4049/jimmunol.180.9.6262. PMID 18424749.
↑ Nakagami Y, Favoreto S, Zhen G, Park SW, Nguyenvu LT, Kuperman DA, Dolganov GM, Huang X, Boushey HA, Avila PC, Erle DJ (August 2008). "The epithelial anion transporter pendrin is induced by allergy and rhinovirus infection, regulates airway surface liquid, and increases airway reactivity and inflammation in an asthma model". Journal of Immunology. 181 (3): 2203–10. doi:10.4049/jimmunol.181.3.2203. PMC 2491716. PMID 18641360.