The expression of wild-type pendrin (SLC26A4) in human embryonic kidney (HEK 293 Phoenix) cells leads to the activation of cationic currents
Author(s) -
Silvia Dossena,
Antonella Maccagni,
Valeria Vezzoli,
Claudia Bazzini,
Maria Lisa Garavaglia,
G. Meyer,
Johannes Fürst,
Markus Ritter,
Laura Fugazzola,
Luca Persani,
Patrick Zorowka,
Carlo Storelli,
Paolo BeckPeccoz,
Guido Fernando Botta,
Markus Paulmichl
Publication year - 2005
Publication title -
european journal of endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 148
eISSN - 1479-683X
pISSN - 0804-4643
DOI - 10.1530/eje.1.02018
Subject(s) - pendrin , hek 293 cells , chemistry , endocrinology , medicine , biophysics , inner ear , chloride channel , reabsorption , microbiology and biotechnology , kidney , biology , biochemistry , anatomy , receptor , gene , transporter
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. Malfunction of SLC26A4 leads to Pendred syndrome, characterized by mild thyroid dysfunction often associated with goiter and/or prelingual deafness. The precise function of the SLC26A4 protein, however, is still elusive. An open question is still whether the SLC26A4-induced ion exchange mechanism is electrogenic or electroneutral. Recently, it has been shown that human pendrin expressed in monkey cells leads to chloride currents.
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