Ginter CS - Search Results

1

The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance.

Dohán O, De la Vieja A, Paroder V, Riedel C, Artani M, Reed M, Ginter CS, Carrasco N. Dohán O, et al. Among authors: ginter cs. Endocr Rev. 2003 Feb;24(1):48-77. doi: 10.1210/er.2001-0029. Endocr Rev. 2003. PMID: 12588808 Review.

2

The Q267E mutation in the sodium/iodide symporter (NIS) causes congenital iodide transport defect (ITD) by decreasing the NIS turnover number.

De La Vieja A, Ginter CS, Carrasco N. De La Vieja A, et al. Among authors: ginter cs. J Cell Sci. 2004 Feb 15;117(Pt 5):677-87. doi: 10.1242/jcs.00898. Epub 2004 Jan 20. J Cell Sci. 2004. PMID: 14734652

3

Molecular analysis of a congenital iodide transport defect: G543E impairs maturation and trafficking of the Na+/I- symporter.

De la Vieja A, Ginter CS, Carrasco N. De la Vieja A, et al. Among authors: ginter cs. Mol Endocrinol. 2005 Nov;19(11):2847-58. doi: 10.1210/me.2005-0162. Epub 2005 Jun 23. Mol Endocrinol. 2005. PMID: 15976004

4

Amino acid residues in transmembrane segment IX of the Na+/I- symporter play a role in its Na+ dependence and are critical for transport activity.

De la Vieja A, Reed MD, Ginter CS, Carrasco N. De la Vieja A, et al. Among authors: ginter cs. J Biol Chem. 2007 Aug 31;282(35):25290-8. doi: 10.1074/jbc.M700147200. Epub 2007 Jul 2. J Biol Chem. 2007. PMID: 17606623 Free article.

5

Molecular characterization of V59E NIS, a Na+/I- symporter mutant that causes congenital I- transport defect.

Reed-Tsur MD, De la Vieja A, Ginter CS, Carrasco N. Reed-Tsur MD, et al. Among authors: ginter cs. Endocrinology. 2008 Jun;149(6):3077-84. doi: 10.1210/en.2008-0027. Epub 2008 Mar 13. Endocrinology. 2008. PMID: 18339708 Free PMC article.

6

The iodide-transport-defect-causing mutation R124H: a δ-amino group at position 124 is critical for maturation and trafficking of the Na+/I- symporter.

Paroder V, Nicola JP, Ginter CS, Carrasco N. Paroder V, et al. Among authors: ginter cs. J Cell Sci. 2013 Aug 1;126(Pt 15):3305-13. doi: 10.1242/jcs.120246. Epub 2013 May 20. J Cell Sci. 2013. PMID: 23690546 Free PMC article.

7

Na(+)/I(-) symporter activity requires a small and uncharged amino acid residue at position 395.

Dohán O, Gavrielides MV, Ginter C, Amzel LM, Carrasco N. Dohán O, et al. Mol Endocrinol. 2002 Aug;16(8):1893-902. doi: 10.1210/me.2002-0071. Mol Endocrinol. 2002. PMID: 12145342

8

Identification of a structural requirement for thyroid Na+/I- symporter (NIS) function from analysis of a mutation that causes human congenital hypothyroidism.

Levy O, Ginter CS, De la Vieja A, Levy D, Carrasco N. Levy O, et al. Among authors: ginter cs. FEBS Lett. 1998 Jun 5;429(1):36-40. doi: 10.1016/s0014-5793(98)00522-5. FEBS Lett. 1998. PMID: 9657379 Free article.

9

N-linked glycosylation of the thyroid Na+/I- symporter (NIS). Implications for its secondary structure model.

Levy O, De la Vieja A, Ginter CS, Riedel C, Dai G, Carrasco N. Levy O, et al. Among authors: ginter cs. J Biol Chem. 1998 Aug 28;273(35):22657-63. doi: 10.1074/jbc.273.35.22657. J Biol Chem. 1998. PMID: 9712895 Free article.

10

Journey of the iodide transporter NIS: from its molecular identification to its clinical role in cancer.

Riedel C, Dohán O, De la Vieja A, Ginter CS, Carrasco N. Riedel C, et al. Among authors: ginter cs. Trends Biochem Sci. 2001 Aug;26(8):490-6. doi: 10.1016/s0968-0004(01)01904-1. Trends Biochem Sci. 2001. PMID: 11504625 Review.

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