' '
Deutsch | English    

Forschungsdatenbank PMU-SQQUID

The expression of wild-type pendrin (SLC26A4) in human embryonic kidney (HEK 293 Phoenix) cells leads to the activation of cationic currents.
Dossena, S; Maccagni, A; Vezzoli, V; Bazzini, C; Garavaglia, ML; Meyer, G; Fürst, J; Ritter, M; Fugazzola, L; Persani, L; Zorowka, P; Storelli, C; Beck-Peccoz, P; Bottà, G; Paulmichl, M;
Eur J Endocrinol. 2005; 153(5): 693-699.
Originalarbeiten (Zeitschrift)

PMU-Autor/inn/en

Dossena Silvia
Paulmichl Markus
Ritter Markus

Abstract

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.


Useful keywords (using NLM MeSH Indexing)

Cations/metabolism*

Cell Line

Chloride Channels/physiology

Electric Conductivity

Humans

Ion Channels/physiology*

Membrane Transport Proteins/metabolism*

Patch-Clamp Techniques

Potassium Channels, Voltage-Gated/physiology