甲状腺激素的nongenomic行动机制。
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戴维斯PJ,伦纳德杰,戴维斯FB
甲状腺激素的nongenomic行动机制。
Neuroendocrinol前面。2008年5月,29 (2):211 - 8。doi: 10.1016 / j.yfrne.2007.09.003。Epub 2007 10月5。
- PubMed ID
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17983645 (在PubMed]
- 文摘
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甲状腺激素的nongenomic行为需要质膜受体或核受体位于细胞质。质膜受体位于整合素alphaVbeta3 Arg-Gly-Asp识别现场重要绑定整合素的细胞外基质蛋白。甲状腺素(T(4))是绑定在这个网站更大的亲和力比3,5,3 ' -triiodo-l-thyronine (T (3))。增殖蛋白激酶(MAPK;ERK1/2)能传感激素信号到复杂的细胞/核事件包括血管生成和肿瘤细胞增殖。代理整合素受体和细胞没有条目,甲状腺激素可以促进ERK1/2-dependent丝氨酸磷酸化核甲状腺激素receptor-beta1 (TRbeta1)和de-repress后者。还整合素受体介导的行为激素在细胞内的蛋白质贩运和质膜离子泵,包括钠/蛋白质逆向转运。Tetraiodothyroacetic (tetrac)是一个T(4)模拟抑制绑定iodothyronines整合素受体和受体参与的调查细胞行为的荷尔蒙。Tetrac块甲状腺激素对血管生成和癌症细胞增殖的影响。作用于一种截断的核TRalpha1 (TRDeltaalpha1)位于细胞质中,T(4)和3,3 ',5 '三碘甲状腺氨酸(反向T(3)),但不是T(3),导致转换的可溶性纤维(F)肌动蛋白肌动蛋白,对细胞活性很重要,例如,在细胞,如神经胶质和神经元。 Normal development of the central nervous system requires such motility. TRbeta1 in cytoplasm mediates action of T(3) on expression of certain genes via phosphatidylinositol 3-kinase (PI 3-K) and the protein kinase B/Akt pathway. PI 3-K and, possibly, cytoplasmic TRbeta1 are involved in stimulation by T(3) of insertion of Na,K-ATPase in the plasma membrane and of increase in activity of this pump. Because ambient thyroid hormone levels are constant in the euthyroid intact organism, these nongenomic hormone actions are likely to be contributors to basal rate-setting of transcription of certain genes and of complex cellular events such as angiogenesis and cancer cell proliferation.