Literature DB >> 22116359

Identification of allelic variants of pendrin (SLC26A4) with loss and gain of function.

Silvia Dossena1, Aigerim Bizhanova, Charity Nofziger, Emanuele Bernardinelli, Josef Ramsauer, Peter Kopp, Markus Paulmichl.   

Abstract

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. Loss or reduction in the function of pendrin results in both syndromic (Pendred syndrome) and non-syndromic (non-syndromic enlarged vestibular aqueduct (ns-EVA)) hearing loss. Factors inducing an up-regulation of pendrin in the kidney and the lung may have an impact on the pathogenesis of hypertension, chronic obstructive pulmonary disease (COPD) and asthma. Here we characterize the ion transport activity of wild-type (WT) pendrin and seven of its allelic variants selected among those reported in the single nucleotide polymorphisms data base (dbSNPs), some of which were previously identified in a cohort of individuals with normal hearing or deaf patients belonging to the Spanish population.
METHODS: WT and mutated pendrin allelic variants were functionally characterized in a heterologous over-expression system by means of fluorometric methods evaluating the I(-)/Cl(-) and Cl(-)/OH(-) exchange and an assay evaluating the efflux of radiolabeled iodide.
RESULTS: The transport activity of pendrin P70L, P301L and F667C is completely abolished; pendrin V609G and D687Y allelic variants are functionally impaired but retain significant transport. Pendrin F354S activity is indistinguishable from WT, while pendrin V88I and G740S exhibit a gain of function.
CONCLUSION: Amino acid substitutions involving a proline always result in a severe loss of function of pendrin. Two hyperfunctional allelic variants (V88I, G740S) have been identified, and they may have a contributing role in the pathogenesis of hypertension, COPD and asthma.
Copyright © 2011 S. Karger AG, Basel.

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Year:  2011        PMID: 22116359      PMCID: PMC3709191          DOI: 10.1159/000335108

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


  51 in total

1.  Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion.

Authors:  I E Royaux; S M Wall; L P Karniski; L A Everett; K Suzuki; M A Knepper; E D Green
Journal:  Proc Natl Acad Sci U S A       Date:  2001-03-27       Impact factor: 11.205

2.  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.

Authors:  I E Royaux; K Suzuki; A Mori; R Katoh; L A Everett; L D Kohn; E D Green
Journal:  Endocrinology       Date:  2000-02       Impact factor: 4.736

3.  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.

Authors:  Yasuhiro Nakagami; Silvio Favoreto; Guohua Zhen; Sung-Woo Park; Louis T Nguyenvu; Douglas A Kuperman; Gregory M Dolganov; Xiaozhu Huang; Homer A Boushey; Pedro C Avila; David J Erle
Journal:  J Immunol       Date:  2008-08-01       Impact factor: 5.422

4.  Pendrin: an apical Cl-/OH-/HCO3- exchanger in the kidney cortex.

Authors:  M Soleimani; T Greeley; S Petrovic; Z Wang; H Amlal; P Kopp; C E Burnham
Journal:  Am J Physiol Renal Physiol       Date:  2001-02

5.  Molecular analysis of the Pendred's syndrome gene and magnetic resonance imaging studies of the inner ear are essential for the diagnosis of true Pendred's syndrome.

Authors:  L Fugazzola; D Mannavola; N Cerutti; M Maghnie; F Pagella; P Bianchi; G Weber; L Persani; P Beck-Peccoz
Journal:  J Clin Endocrinol Metab       Date:  2000-07       Impact factor: 5.958

Review 6.  Molecular and functional characterization of human pendrin and its allelic variants.

Authors:  Silvia Dossena; Charity Nofziger; Grazia Tamma; Emanuele Bernardinelli; Simone Vanoni; Christoph Nowak; Elisabeth Grabmayer; Sonja Kössler; Susanne Stephan; Wolfgang Patsch; Markus Paulmichl
Journal:  Cell Physiol Biochem       Date:  2011-11-18

7.  Green fluorescent protein-based halide indicators with improved chloride and iodide affinities.

Authors:  L J Galietta; P M Haggie; A S Verkman
Journal:  FEBS Lett       Date:  2001-06-22       Impact factor: 4.124

8.  High phenotypic intrafamilial variability in patients with Pendred syndrome and a novel duplication in the SLC26A4 gene: clinical characterization and functional studies of the mutated SLC26A4 protein.

Authors:  Laura Fugazzola; Valentina Cirello; Silvia Dossena; Simona Rodighiero; Marina Muzza; Pierangela Castorina; Faustina Lalatta; Umberto Ambrosetti; Paolo Beck-Peccoz; Guido Bottà; Markus Paulmichl
Journal:  Eur J Endocrinol       Date:  2007-09       Impact factor: 6.664

9.  The Slc26a4 transporter functions as an electroneutral Cl-/I-/HCO3- exchanger: role of Slc26a4 and Slc26a6 in I- and HCO3- secretion and in regulation of CFTR in the parotid duct.

Authors:  Nikolay Shcheynikov; Dongki Yang; Youxue Wang; Weizong Zeng; Lawrence P Karniski; Insuk So; Susan M Wall; Shmuel Muallem
Journal:  J Physiol       Date:  2008-06-19       Impact factor: 5.182

10.  Identification of pendrin as a common mediator for mucus production in bronchial asthma and chronic obstructive pulmonary disease.

Authors:  Isao Nakao; Sachiko Kanaji; Shoichiro Ohta; Hidetomo Matsushita; Kazuhiko Arima; Noriko Yuyama; Mutsuo Yamaya; Katsutoshi Nakayama; Hiroshi Kubo; Mika Watanabe; Hironori Sagara; Kumiya Sugiyama; Hiroyuki Tanaka; Shuji Toda; Hiroaki Hayashi; Hiromasa Inoue; Tomoaki Hoshino; Aya Shiraki; Makoto Inoue; Koichi Suzuki; Hisamichi Aizawa; Satoshi Okinami; Hiroichi Nagai; Mamoru Hasegawa; Takeshi Fukuda; Eric D Green; Kenji Izuhara
Journal:  J Immunol       Date:  2008-05-01       Impact factor: 5.422

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  14 in total

1.  Reduction of Cellular Expression Levels Is a Common Feature of Functionally Affected Pendrin (SLC26A4) Protein Variants.

Authors:  Vanessa C S de Moraes; Emanuele Bernardinelli; Nathalia Zocal; Jhonathan A Fernandez; Charity Nofziger; Arthur M Castilho; Edi L Sartorato; Markus Paulmichl; Silvia Dossena
Journal:  Mol Med       Date:  2016-01-04       Impact factor: 6.354

Review 2.  Novel therapies for the treatment of pertussis disease.

Authors:  Karen M Scanlon; Ciaran Skerry; Nicholas H Carbonetti
Journal:  Pathog Dis       Date:  2015-09-21       Impact factor: 3.166

3.  Expert specification of the ACMG/AMP variant interpretation guidelines for genetic hearing loss.

Authors:  Andrea M Oza; Marina T DiStefano; Sarah E Hemphill; Brandon J Cushman; Andrew R Grant; Rebecca K Siegert; Jun Shen; Alex Chapin; Nicole J Boczek; Lisa A Schimmenti; Jaclyn B Murry; Linda Hasadsri; Kiyomitsu Nara; Margaret Kenna; Kevin T Booth; Hela Azaiez; Andrew Griffith; Karen B Avraham; Hannie Kremer; Heidi L Rehm; Sami S Amr; Ahmad N Abou Tayoun
Journal:  Hum Mutat       Date:  2018-11       Impact factor: 4.878

4.  Systematic quantification of the anion transport function of pendrin (SLC26A4) and its disease-associated variants.

Authors:  Koichiro Wasano; Satoe Takahashi; Samuel K Rosenberg; Takashi Kojima; Hideki Mutai; Tatsuo Matsunaga; Kaoru Ogawa; Kazuaki Homma
Journal:  Hum Mutat       Date:  2019-10-26       Impact factor: 4.878

5.  Iodide excess regulates its own efflux: a possible involvement of pendrin.

Authors:  Jamile Calil-Silveira; Caroline Serrano-Nascimento; Peter Andreas Kopp; Maria Tereza Nunes
Journal:  Am J Physiol Cell Physiol       Date:  2016-01-20       Impact factor: 4.249

6.  American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.

Authors:  Antonio C Bianco; Grant Anderson; Douglas Forrest; Valerie Anne Galton; Balázs Gereben; Brian W Kim; Peter A Kopp; Xiao Hui Liao; Maria Jesus Obregon; Robin P Peeters; Samuel Refetoff; David S Sharlin; Warner S Simonides; Roy E Weiss; Graham R Williams
Journal:  Thyroid       Date:  2013-12-12       Impact factor: 6.568

7.  Screening of genetic alterations related to non-syndromic hearing loss using MassARRAY iPLEX® technology.

Authors:  Maria Carolina Costa Melo Svidnicki; Sueli Matilde Silva-Costa; Priscila Zonzini Ramos; Nathalia Zocal Pereira dos Santos; Fábio Tadeu Arrojo Martins; Arthur Menino Castilho; Edi Lúcia Sartorato
Journal:  BMC Med Genet       Date:  2015-09-23       Impact factor: 2.103

8.  Optimization of simultaneous screening of the main mutations involved in non-syndromic deafness using the TaqMan® OpenArray™ Genotyping platform.

Authors:  Fábio Tadeu Arrojo Martins; Priscila Zonzini Ramos; Maria Carolina Costa Melo Svidnicki; Arthur Menino Castilho; Edi Lúcia Sartorato
Journal:  BMC Med Genet       Date:  2013-10-24       Impact factor: 2.103

9.  Mutation Analysis of the Common Deafness Genes in Patients with Nonsyndromic Hearing Loss in Linyi by SNPscan Assay.

Authors:  Fengguo Zhang; Yun Xiao; Lei Xu; Xue Zhang; Guodong Zhang; Jianfeng Li; Huaiqing Lv; Xiaohui Bai; Haibo Wang
Journal:  Biomed Res Int       Date:  2016-05-09       Impact factor: 3.411

10.  Functional Testing of SLC26A4 Variants-Clinical and Molecular Analysis of a Cohort with Enlarged Vestibular Aqueduct from Austria.

Authors:  Sebastian Roesch; Emanuele Bernardinelli; Charity Nofziger; Miklós Tóth; Wolfgang Patsch; Gerd Rasp; Markus Paulmichl; Silvia Dossena
Journal:  Int J Mol Sci       Date:  2018-01-10       Impact factor: 5.923

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