TSHR脱敏
TSHR与活化型G-蛋白（GS）偶联，GS激活腺苷酸环化酶生成cAMP和Gq/11，cAMP和Gq/11激活PKC，PKC催化1，4，5-三磷酸肌醇的产生从而介导TSH的生物学效应。然而，持续的TSH刺激将会下调胞内cAMP水平，使TSHR介导的生物学效应终止，这种由配体持续作用导致的受体失活现象被称为“受体脱敏”（Desensitization）。TSHR脱敏现象是甲状腺细胞特异的，在其他组织细胞中表达的TSHR可与TSH结合并发挥有效功能，但并不会发生脱敏现象，就此推测TSHR的脱敏是由甲状腺细胞特有的脱敏蛋白介导的。
G-蛋白偶联受体激酶或蛋白激酶A介导的特定氨基酸残基的磷酸化是某些G-蛋白偶联受体脱敏的主要机制。相比于其他G-蛋白偶联受体，TSH受体细胞内环状结构和羧基端结构域含有的可被磷酸化修饰的丝氨酸/苏氨酸残基较少；TSH的持续作用使TSHR快速脱敏，可能有微弱的磷酸化作用的参与。TSHR mRNA和蛋白分子的代谢周期很长而脱敏化过程非常微弱。给予小鼠慢性刺激性单克隆抗体输注可导致明显的甲亢，但并没有TSHR脱敏的征象。运用转染了cAMP感应器的小鼠甲状腺细胞发现，细胞内转染过表达的TSHR与TSH结合后可发生内化并定位于细胞内涵体中，TSH刺激后发生内化的TSHR仍对Gαs有激活作用[47]。这可能充分解释了TSH分泌性垂体瘤伴发Graves病甲状腺毒症的机制。
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