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(A) Schematic representation of major thyroid hormone receptors (TRα, β) domains and functional sub-regions. (B) General model for genomic and non-genomic actions of TH in both adult and fetus; Schematic representation of thyroid hormones (THs; T4 and T3) genomic actions, initiated at the nuclear receptors (TRβ), and non-genomic actions, initiated at cytoplasmatic receptors (TRβ, TRα) and at the plasma membrane on the membrane receptors, particularly integrin αvβ3 receptor. T4 binding (but not T3) to cytoplasmic TRα may cause a change of state of actin. T3 binding (but not T4) to cytoplasmic TRβ activates the phosphatidylinositol 3-kinase (PI-3K) pathway leading to alteration in membrane ion pumps and to transcription of specific genes. TH binding to the integrin receptor results in activation of mitogen-activated protein kinase (MAPK/ERK1/2). Phosphorylated MAPK (pMAPK) translocates to the nucleus where it phosphorylates transcription factors including thyroid receptors (TRβ), estrogen receptor (ER) and signal transducer activators of transcription (STAT). Generally, activity is regulated by an exchange of corepressor (CoR) and coactivator (CoA) complexes.  

(A) Schematic representation of major thyroid hormone receptors (TRα, β) domains and functional sub-regions. (B) General model for genomic and non-genomic actions of TH in both adult and fetus; Schematic representation of thyroid hormones (THs; T4 and T3) genomic actions, initiated at the nuclear receptors (TRβ), and non-genomic actions, initiated at cytoplasmatic receptors (TRβ, TRα) and at the plasma membrane on the membrane receptors, particularly integrin αvβ3 receptor. T4 binding (but not T3) to cytoplasmic TRα may cause a change of state of actin. T3 binding (but not T4) to cytoplasmic TRβ activates the phosphatidylinositol 3-kinase (PI-3K) pathway leading to alteration in membrane ion pumps and to transcription of specific genes. TH binding to the integrin receptor results in activation of mitogen-activated protein kinase (MAPK/ERK1/2). Phosphorylated MAPK (pMAPK) translocates to the nucleus where it phosphorylates transcription factors including thyroid receptors (TRβ), estrogen receptor (ER) and signal transducer activators of transcription (STAT). Generally, activity is regulated by an exchange of corepressor (CoR) and coactivator (CoA) complexes.  

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Context 1
... the thyroid gland predominantly secretes T4, T3 is the most active TH, since it has a higher affinity by the nuclear thyroid hormone receptors (TRs; α, β) ( Figure 2A) [75], which mediate most actions of these hormones [72,73]. THs are released by the thyroid gland to the circulation where they are carried bound to proteins such as thyroxin binding globulin (TBG), transthyretin (TTR) or serum albumin (Table 4) [74]. ...
Context 2
... general, thyrotoxicosis is the syndrome resulting from an excess of circulating free T4 and/or free T3 [147,148]. Babies likely to become hyperthyroid have the highest TSH receptor antibody titer whereas if TSH receptor antibodies are not detectable, the baby is most unlikely to become hyperthyroid ( Figure 3) [1,2,149]. In the latter case, it can be anticipated that the baby will be euthyroid, have transient hypothalamic-pituitary suppression or have a transiently elevated TSH, depending on the relative contribution of maternal hyperthyroidism versus the effects of maternal antithyroid medication, respectively [150]. ...