1 Pharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences , Albany, New York.
Thyroid. 2013 Dec;23(12):1503-9. doi: 10.1089/thy.2013.0280. Epub 2013 Nov 5.
At thyroid hormone response elements on specific genes, complexes of nuclear thyroid hormone receptors (TRs) and 3,5,3'-triiodo-L-thyronine (T(3)), coactivator or corepressor nucleoproteins, and histone acetylases or deacetylases mediate genomic effects of the hormone. Nongenomic effects of the hormone are those whose initiation does not primarily depend upon formation of the TR-T(3) complex. Among the nongenomic effects of thyroid hormone are a set of actions initiated at a cell surface receptor on integrin αvβ3 that are relevant to a) intracellular trafficking of proteins, including TRβ1, b) serine phosphorylation and acetylation of this nuclear receptor, c) assembly within the nucleus of complexes of coactivators and corepressor, and d) transcription of specific genes, including that for TRβ1. These actions initiated at αvβ3 are reviewed here and appear to be adjunctive to the genomic actions of the TR-T(3) complex.
在特定基因的甲状腺激素反应元件上，核甲状腺激素受体 (TR) 与 3,5,3'-三碘甲腺原氨酸 (T(3))、共激活剂或核心抑制剂核蛋白、组蛋白乙酰转移酶或去乙酰化酶的复合物介导激素的基因组效应。激素的非基因组效应是指其起始并不主要依赖于 TR-T(3) 复合物的形成。甲状腺激素的非基因组效应之一是一组在整合素 αvβ3 上的细胞表面受体启动的作用，这些作用与 a) 蛋白质的细胞内运输有关，包括 TRβ1，b) 该核受体的丝氨酸磷酸化和乙酰化，c) 共激活剂和核心抑制剂复合物在核内的组装，以及 d) 特定基因的转录，包括 TRβ1。本文回顾了这些在 αvβ3 上启动的作用，它们似乎是 TR-T(3) 复合物的基因组作用的辅助。
