???pagination.result.count???
???pagination.result.page???
1
Hypo-functional SLC26A4 variants associated with nonsyndromic hearing loss and enlargement of the vestibular aqueduct: genotype-phenotype correlation or coincidental polymorphisms? , Choi BY., Hum Mutat. April 1, 2009; 30 (4): 599-608.
[Evidence of a novel gene for the LAV-syndrome]. , Birkenhäger R., Laryngorhinootologie. February 1, 2007; 86 (2): 102-6.
[Identification of two heterozygous mutations in the SLC26A4/PDS gene in a family with Pendred-syndrome]. , Birkenhäger R., Laryngorhinootologie. December 1, 2004; 83 (12): 831-5.
Functional characterization of pendrin in a polarized cell system. Evidence for pendrin-mediated apical iodide efflux. , Gillam MP., J Biol Chem. March 26, 2004; 279 (13): 13004-10.
Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells. , Yoshida A., J Clin Endocrinol Metab. July 1, 2002; 87 (7): 3356-61.
Functional differences of the PDS gene product are associated with phenotypic variation in patients with Pendred syndrome and non-syndromic hearing loss ( DFNB4). , Scott DA., Hum Mol Genet. July 1, 2000; 9 (11): 1709-15.
Human pendrin expressed in Xenopus laevis oocytes mediates chloride/formate exchange. , Scott DA., Am J Physiol Cell Physiol. January 1, 2000; 278 (1): C207-11.
The Pendred syndrome gene encodes a chloride-iodide transport protein. , Scott DA., Nat Genet. April 1, 1999; 21 (4): 440-3.