Thyroid Hormone Beta Receptor Mutation Causes Renal Dysfunction and Impairment of ClC-2 Chloride Channel Expression in Mouse Kidney | Zendy

Aline Cristina Gomes Santos | Zendy; Aline Cristina Gomes | Zendy; Letícia Aragão Santiago | Zendy; Horacio J. Novaira | Zendy; Tania Maria OrtigaCarvalho | Zendy; Marcelo M. Morales | Zendy

Open Access

Thyroid Hormone Beta Receptor Mutation Causes Renal Dysfunction and Impairment of ClC-2 Chloride Channel Expression in Mouse Kidney

Author(s) -

Aline Cristina Gomes Santos,

Aline Cristina Gomes,

Letícia Aragão Santiago,

Horacio J. Novaira,

Tania Maria OrtigaCarvalho,

Marcelo M. Morales

Publication year - 2010

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000320522

Subject(s) - endocrinology , medicine , thyroid , kidney , thyroid hormone receptor beta , thyroid hormone receptor , hormone , receptor , fractional excretion of sodium , chloride channel , biology , chemistry , hormone receptor , microbiology and biotechnology , cancer , breast cancer

Mutations in the thyroid hormone receptor beta (TR-beta) gene result in resistance to thyroid hormone (RTH). Mutation Delta337T in the TR-beta gene has been shown to have the characteristics of RTH syndrome in mice. The aim of this work was to study the possible involvement of TR-beta receptor in thyroid modulation of ClC-2 in mouse kidney.

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