Faculty Opinions recommendation of SKP2 Activation by Thyroid Hormone Receptor β2 bypasses Rb-Dependent Proliferation in Rb-Deficient Cells.
0
Citation
0
Reference
10
Related Paper
Keywords:
Thyroid hormone receptor
SKP2
Experimental acute toxic hepatitis causes functional reconstruction of the thyroid gland accompanied by intensified levels of total iodine and its hormonal compounds in blood. In most of non-thyroid tissues a decrease in the total and hormonal iodine content is revealed, but in kidneys these indices are considerably higher. The level of the nonhormonal iodine compounds in blood and tissues under study does not essentially vary and only in the liver, heart and lungs the expressed lowering of inorganic iodides is observed.
Acute hepatitis
Cite
Citations (0)
Normal thyroid hormone level is essential to maintain the normal physiologic function of the human body. Disturbances of these hormone levels have variable clinical manifestations ranging from asymptomatic to severe illness. Resistance to thyroid hormone (RTH) is a syndrome characterized by reduced intracellular action of T3, the active thyroid hormone. It is a rare autosomal dominant condition and occurs mostly due to heterogeneous mutations in the thyroid hormone receptor. Other causes of RTH include thyroid hormone cell membrane transport defect and thyroid hormone metabolism defect. Affected individuals present with symptoms of both increased and decreased thyroid hormone action, depending on the tissue’s predominant receptor isoform expression, the magnitude of hormonal resistance, and the effectiveness of compensatory mechanisms. Here, we share our experience in diagnosing a case of RTH confirmed with a genetic test and found to have sequence variant mutation that is not well described in the literature previously due to the absence of genetic conclusive evidence.
Thyroid hormone receptor
Cite
Citations (2)
Second messenger system
Cell surface receptor
Cite
Citations (6)
Thyroid hormone receptor
Homeostasis
Cite
Citations (166)
Cell surface receptor
Cell membrane
Cite
Citations (47)
Despite clinical evidence that thyroid hormone is essential for brain development before birth, effects of thyroid hormone on the fetal brain have been largely unexplored. One mechanism of thyroid hormone action is regulation of gene expression, because thyroid hormone receptors (TRs) are ligand-activated transcription factors. We used differential display to identify genes affected by acute T 4 administration to the dam before the onset of fetal thyroid function. Eight of the 11 genes that we identified were selectively expressed in brain areas known to contain TRs, indicating that these genes were directly regulated by thyroid hormone. Using in situ hybridization, we confirmed that the cortical expression of both neuroendocrine-specific protein (NSP) and Oct-1 was affected by changes in maternal thyroid status. Additionally, we demonstrated that both NSP and Oct-1 were expressed in the adult brain and that their responsiveness to thyroid hormone was retained. These data are the first to identify thyroid hormone-responsive genes in the fetal brain.
Thyroid hormone receptor
Cite
Citations (122)
Cite
Citations (0)
Thyroid hormones (TH) play a key role in energy homeostasis throughout life. Thyroid hormone production and secretion by the thyroid gland is regulated via the hypothalamus-pituitary-thyroid (HPT)-axis. Thyroid hormone has to be transported into the cell, where it can bind to the thyroid hormone receptor (TR) in the nucleus to exert its effect on cellular gene-transcription. Mutations in both the THRA and THRB gene have been described, each inducing a characteristic phenotype clearly showing the selective effect of an excess or shortage of thyroid hormone in specific TRα and TRβ regulated organs. Profound changes in thyroid hormone metabolism occur during a variety of non-thyroidal illnesses, each associated with reduced TR expression in a tissue-specific manner. However, thyroid hormone action at the tissue level during illness is not a simple reflection of the extent of TR expression as illness has additional differential effects on local thyroid hormone availability in various organs.
Thyroid hormone receptor
Endocrine gland
Thyroid disease
Hypothalamic–pituitary–thyroid axis
Cite
Citations (14)
BAUMANN (1) was the first to recognize that the thyroid gland had the capacity to retain and store iodine. Other workers (2, 3) have shown a positive correlation between functional states of the thyroid gland and thyroidal iodine stores. Since these studies were performed in glands which were removed at operation or at the autopsy table, the data so derived were not applicable to the living patient except in a general way. It is apparent that an experimental method which would allow such studies in vivo would be extremely helpful, both in understanding the pathogenesis of thyroid disease and in helping to determine the type and amount of therapy required. Tracer doses of radioactive iodine which are fixed in the thyroid gland can be released into the blood stream along with stable hormonal iodine in response to administered thyroid-stimulating hormone (TSH). By comparing the specific radioactivity of the newly secreted hormone with the thyroidal content of I131, it is possible to estimate the hormonal stores of the intact human gland. Becker et al. (4) employed this technique in 3 eu thyroid subjects and assumed that after five to eight days the specific activity of the circulating serum protein-bound iodine (PBI) was equal to that of the thyoidal compartment. In the present study the specific radioactivity of the newly secreted PBI was determined directly, so that equilibration of thyroidal and extrathyroidal PBI compartments was not necessary for valid hormonal store calculations.
Cite
Citations (14)
The effects of thyroid hormones are mediated through nuclear receptor proteins that modulate the transcription of specific genes in target cells. We previously isolated cDNAs encoding two different mammalian thyroid hormone receptors, one from human placenta (hTR beta) and the other from rat brain (rTR alpha), and showed that their in vitro translation products bind thyroid hormones with the characteritistic affinities of the native thyroid hormone receptor. We now demonstrate that both of the cloned receptors activate transcription from a thyroid hormone-responsive promoter in a hormone-dependent manner, with rTR alpha eliciting a greater response than hTR beta. The putative functional domains of the thyroid hormone receptors were examined by creating chimeric thyroid hormone/glucocorticoid receptors, producing receptors with hybrid functional properties. These experiments support the proposal that the thyroid hormone receptors are composed of interchangeable functional domains, and indicate that the mechanism of hormone-inducible gene regulation has been conserved in steroid and thyroid hormone receptors.
Thyroid hormone receptor
Sex hormone receptor
Hormone response element
Steroid hormone
Growth-hormone-releasing hormone receptor
Cite
Citations (154)