Thyroid-specific and hormone-dependent expression of rat thyroglobulin promoter fused with bacterial chloramphenicol acetyltransferase gene in transgenic mice

Skinner, Cheryl A.; Kelly, Douglas G.; Kao, Li Cheng; Nayfeh, Shihadeh N.; Popko, Brian; Chae, Claudia U.

doi:10.1016/0303-7207(92)90098-q

Cited by 6 publications

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“…The tissue specificity of the bovine thyroglobulin gene promoter was further demonstrated in our subsequent models (see below), since primary abnormalities were in all cases restricted to the thyroid gland. A similar thyroid specific expression was obtained by Skinner et al, (1992), using a shorter fragment (168 bp) of the rat thyroglobulin gene promoter. Santelli et al, (1993) also reported the thyroid specific targeting of a CAT hybrid gene under control of the rat thyroglobulin gene promoter.…”

Section: Introductionsupporting

confidence: 56%

Transgenic models for proliferative and hyperfunctional thyroid diseases

Ledent

Coppée²,

Dumont³

et al. 2009

Exp Clin Endocrinol Diabetes

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Mouse transgenic models that develop thyroid diseases were generated. All transgenes were driven by the thyroid specific promoter of the thyroglobulin gene. The tissue specificity of the promoter was investigated by using the bacterial chloramphenicol acetyl transferase gene as reporter. The expression of an adenosine A2a receptor resulted in the permanent activation of the cAMP cascade. As a consequence, the transgenic mice developed severe hyperthyroidism and a large goiter, demonstrating in vivo the role of the cAMP cascade in the promotion of both function and proliferation of the thyroid cell. These mice constitute a model for autonomous hyperfunctional adenoma and non-autoimmune familial hyperthyroidism, where mutant thyrotropin receptors stimulate the cAMP cascade constitutively. In another transgenic model, the function of the retinoblastoma susceptibility gene product RB1 (and of related proteins) was inhibited by expression of the E7 oncoprotein of human papillomavirus type 16. The result was the development of a differentiated and normofunctional colloid goiter, with the progressive development of differentiated malignant lesions. This model suggests the essential role of RB1 and related proteins in the negative control of proliferation that characterizes thyroid cells in the adult. Other transgenic models of thyroid diseases are discussed.

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