The Role of Type 1 and Type 2 5′-Deiodinase in the Pathophysiology of the 3,5,3′-Triiodothyronine Toxicosis of McCune-Albright Syndrome | Zendy

Francesco S. Celi | Zendy; Giuseppe Coppotelli | Zendy; Aaron Chidakel | Zendy; Marilyn Kelly | Zendy; Beth A Brillante | Zendy; Thomas H. Shawker | Zendy; Natasha Cherman | Zendy; Penelope Feuillan | Zendy; Michael T. Collins | Zendy

Open Access

The Role of Type 1 and Type 2 5′-Deiodinase in the Pathophysiology of the 3,5,3′-Triiodothyronine Toxicosis of McCune-Albright Syndrome

Author(s) -

Francesco S. Celi,

Giuseppe Coppotelli,

Aaron Chidakel,

Marilyn Kelly,

Beth A Brillante,

Thomas H. Shawker,

Natasha Cherman,

Penelope Feuillan,

Michael T. Collins

Publication year - 2008

Publication title -

the journal of clinical endocrinology and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.206

H-Index - 353

eISSN - 1945-7197

pISSN - 0021-972X

DOI - 10.1210/jc.2007-2237

Subject(s) - gnas complex locus , mccune–albright syndrome , context (archaeology) , deiodinase , endocrinology , triiodothyronine , medicine , pathophysiology , endocrine system , thyroid , biology , hormone , genetics , precocious puberty , paleontology , gene

McCune-Albright syndrome (MAS) is caused by mutations in GNAS (most often R201C or R201H) leading to constitutive cAMP signaling and multiple endocrine dysfunctions, including morphological and functional thyroid involvement.

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