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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid hormone dependent transcription stimulatory and inhibitory elements exist at the 5'-end of the rat GH (rGH) gene (TSE and TIE, respectively). In this study, the location of the sequences essential for TSE activity was examined using stably transfected GC cells. Because the TIE may influence TSE activity, we investigated TSE activity both on the rGH promoter, in the presence of the TIE, and on the viral thymidine kinase promoter, with the TIE deleted. The results of these studies indicate that the minimum sequences essential for TSE activity exist between positions -194 and -169 of the rGH gene.
Mol Endocrinol 1988 Jun
PMID:Sequences essential for activity of the thyroid hormone responsive transcription stimulatory element of the rat growth hormone gene. 284 60

C-fos promoter activity was examined in FRTL5 rat thyroid cells transiently transfected with a chimeric gene containing the c-fos promoter region linked upstream of the receptor gene chloroamphenicol acetyl transferase (CAT). Thyroid-stimulating hormone (TSH) stimulation of transfected cells increased CAT activity 2- to 3-fold. TSH did not stimulate CAT activity driven by the Rous sarcoma virus (RSV) promoter. Both forskolin and 8-Br-cyclic AMP also stimulated CAT activity, and were not additive with TSH stimulation. The kinetics of c-fos-driven CAT activity in response to TSH and cyclic AMP inducers were similar, and stimulation was reversible. These data therefore provide the first evidence that TSH and cyclic AMP stimulate the activity of the c-fos promoter in FRTL5 cells.
Mol Cell Endocrinol 1988 Aug
PMID:TSH stimulates the activity of the c-fos promoter in FRTL5 rat thyroid cells. 285 Feb 50

Thyroid hormone has a number of effects on cardiovascular and renal function which are shared by the atrial natriuretic peptide (ANP). We attempted to demonstrate a relationship between the two by studying the effects of thyroid hormone on the expression of the ANP gene and the secretion of its encoded protein. Thyroid hormone, when given to thyroidectomized rats, increased plasma ANP levels by approximately 2-fold in both watered and dehydrated animals. Cardiac ANP mRNA in dehydrated animals fell to 25% of that in the water-replete controls. T4 increased cardiac ANP mRNA 3-fold in dehydrated animals, but failed to alter ANP mRNA in those animals allowed free access to water. The effect of thyroid hormone appeared to take place, at least in part, at the level of the ANP-synthesizing cardiocyte. T3, at concentrations ranging from 10(-10)-10(-8) M, increased ANP mRNA levels a maximum of 2-fold in primary cultures of neonatal cardiocytes. Both basal and T3-stimulated ANP transcripts appeared to be identical to their counterparts in the adult atria, as assessed by blot hybridization and S1 nuclease analysis. T3 (10(-8) M) also effected a 2-fold increase in media ANP immunoreactivity. These data indicate that thyroid hormone increases the secretion and genetic expression of ANP in vivo and in vitro and suggests a role for the peptide as a mediator of at least some thyroid hormone effects in the cardiovascular system.
Mol Endocrinol 1987 Mar
PMID:Thyroid hormone increases rat atrial natriuretic peptide messenger ribonucleic acid accumulation in vivo and in vitro. 296 52

Thyroid hormone (10(-11) to 10(-10) M) stimulates plasma membrane Ca2+-ATPase activity in vitro in various tissues, including the human red cell (RBC), by a calmodulin-requiring mechanism. Bepridil and cetiedil are Ca2+ antagonists with an intracellular (calmodulin-antagonist) site of action, as well as an effect on the calcium channel in excitable tissues. We have studied the actions of bepridil and cetiedil on Ca2+-ATPase in a channel-free membrane (RBC) to determine effectiveness of these agents as inhibitors of thyroid hormone action on the enzyme. Dose-response studies showed that thyroid hormone stimulation of Ca2+-ATPase activity in vitro was significantly inhibited by as little as 2 x 10(-5) M bepridil and cetiedil. IC50 values of bepridil and cetiedil for thyroid hormone response of the enzyme were 5 x 10(-5) and 2 x 10(-5) M, respectively, whereas IC50s of these agents for enzyme activity in the absence of thyroid hormone were both 10(-4) M. Progressive addition of purified rat testis calmodulin in vitro (10-150 ng calmodulin/mg membrane protein) restored hormone responsiveness in the presence of bepridil and cetiedil. Binding of labeled thyroid hormone by RBC membranes was unaffected by bepridil and cetiedil (up to 2 x 10(-4) M). Thus, bepridil and cetiedil are Ca2+ antagonists that reversibly inhibit thyroid hormone action on human RBC Ca2+-ATPase by a calmodulin-dependent mechanism. Thyroid hormone effect on Ca2+-ATPase is more susceptible to bepridil and cetiedil inhibition than is basal enzyme activity.
Mol Endocrinol 1987 Feb
PMID:Bepridil and cetiedil reversibly inhibit thyroid hormone stimulation in vitro of human red cell Ca2+-ATPase activity. 297 May 87

In studies on immunogenetic factors in autoimmune thyroid disease, the association among Graves' disease, Hashimoto's disease, HLA and Gm haplotypes was investigated in 37 families in which two or more first degree relatives had Graves' disease. The results showed that two genes linked to HLA and Gm appeared to control susceptibility to Graves' and Hashimoto's disease, respectively, and that the individuals who did not have immunogenetic factors were very unlikely to develop Graves' or Hashimoto's disease. In the second study, the role of HLA-DR antigen expression on thyrocytes was investigated in 18 patients with Graves' disease. It was found that DR-positive thyrocytes increased. DR-positive T-cells (from thyroids and peripheral blood) increased in Graves' disease. Interferon gamma increased DR expression on thyrocytes. The results indicated that these changes may cause a vicious circle to produce and perpetuate autoimmune processes in Graves' disease. Finally, the correlation between thyroids and immunoglobulins was investigated in 11 untreated patients with Graves' disease. Thyroid tissues obtained from untreated patients were incubated in organ culture systems with autologous as well as allogeneic immunoglobulins to observe the release of hormones. The release of hormone was stimulated only by autologous immunoglobulins and it is, therefore, postulated that the role of self-recognition, such as anti-idiotype antibody or anti-MHC antibody is crucial in the pathogenesis of Graves' disease.
Mol Biol Med 1986 Feb
PMID:The interaction of MHC and Gm in liability to autoimmune thyroid disease. 300 22

Recent epidemiological studies in Japan and Sweden have disclosed a high prevalence of transient thyroid dysfunction in women following delivery. These changes seem to reflect an immunoregulatory "rebound" following pregnancy-induced immunosuppression. Thyroid microsomal antibody titers characteristically decrease during pregnancy and increase again after delivery to maximum levels around six months postpartum. At this time some microsomal antibody-positive women develop goitrous hypothyroidism. Subsequently, the microsomal antibody titers fall, reaching the early pregnancy values one year postpartum by which time hypothyroidism subsides. The severity of hypothyroidism is closely related to the titer of microsomal antibody, especially the immunoglobulin G1 subclass of microsomal antibody, and partly predictable from the titer in early pregnancy. The HLA-DR4 antigen was observed in 58% of microsomal antibody-positive Swedish women as compared to 33.7% in the general population (relative risk = 2.71). This association was even stronger in microsomal antibody-positive women who developed postpartum hypothyroidism (69%; relative risk = 4.36). Finally, postpartum thyrotoxicosis with a high radioiodine uptake may occur in women with latent Graves' disease. In these cases changes of TSH-receptor-stimulating antibodies analogous to microsomal antibodies seem to occur.
Mol Biol Med 1986 Apr
PMID:Postpartum thyroid disease. 346 Dec 36

It has been recognized for a long time that changes in hormone secretion can influence cardiac function; however, the biochemical basis for these changes has only recently been clarified. In this review the influences of hormonal status on the contractile protein myosin is discussed. Myosin has a rod-like portion and a globular head and consists of two myosin heavy chains (MHC) and four light chains (LC), two of which are identical. The globular head is the site of an ATP-splitting enzyme, the myosin ATPase, and increases in myosin ATPase activity are closely related to an increased velocity of contraction of the heart. Myosin ATPase activity shows marked response to alterations in thyroid hormone, insulin, glucocorticoid, testosterone and catecholamine levels, but marked animal species differences in this response occur. Thyroid hormone administration to normal rabbits, for example, increases myosin ATPase activity markedly, but the myosin ATPase activity of hyperthyroid rats remains unchanged. In contrast, in hypothyroid rats myosin ATPase activity is markedly decreased but the hypothyroid rabbit shows no such response. These species-related differences in the hormonal response of myosin ATPase activity result from the predominance pattern of specific myosin isoenzymes. In the normal rat heart three myosin isoenzymes, V1, V2 and V3, can be separated electrophoretically. Myosin V1 predominates (70% of total myosin), and has the highest myosin ATPase activity, whereas in rabbits myosin V3, which has a lower myosin ATPase activity, is the predominant isomyosin. Thyroid hormone administration to rabbits induces myosin V1 predominance and therefore increases myosin ATPase activity, whereas in hyperthyroid rats only a small further increase in V1 predominance can occur. The alterations in myosin isoenzyme predominance and myosin ATPase activity are closely correlated to changes in cardiac contractility. Hormone-induced alterations in myosin isoenzyme predominance are mediated through changes in the formation of two isoforms of myosin heavy chain. Changes in the expression of different myosin heavy chain genes are most likely responsible for the thyroid hormone and insulin-induced alterations in myosin isoenzyme predominance. Investigation of the control of myosin heavy chain formation can provide further insights into the hormonal control of a multigene family as well as broaden our understanding of the molecular events which result in altered cardiac contractility.(ABSTRACT TRUNCATED AT 400 WORDS)
Mol Cell Endocrinol 1984 Mar
PMID:Hormonal influences on cardiac myosin ATPase activity and myosin isoenzyme distribution. 623 63

Nuclear pore complexes were analyzed in freeze-fractured replicas of thyroid follicular cells of C3H mice in different physiological states. Thyroid stimulation induced a rapid and simultaneous increase of the nuclear surface and volume and of the total number of pore complexes. The numerical density (Na) of pore complexes increased at the 6th day of stimulation, but after that time the proportion of cells with an increased Na was always higher than the proportion of 3H-labelled nuclei. During thyroid involution, all the nuclear parameters, including the Na, returned to normal values. These results indicate that the total number of pore complexes and their Na are correlated with the cellular activity rather than with the cell cycle. They also suggest that 2 different mechanisms are involved in the generation of pore complexes: first, an addition of new membranes with a low density of pore complexes; later, a formation of new pore complexes in preexisting membranes. However, during involution, parts of the nuclear membranes and pore complexes in the remaining parts disappear synchronously. In freeze-fractured thyroid nuclear membranes, 2 neighbouring pore complexes were always separated by a distance of 105 nm. Clusters of pore complexes were not observed. A comparison of the distances between pore complexes and between randomly generated points never showed any significant differences indicating that pore complexes were randomly distributed.
Mol Cell Endocrinol 1981 Aug
PMID:Morphometry of nuclear pore complexes in thyroid cells during hyperplasia and involution. 727 48

Thyroid hormone receptor acts as a hormone-dependent transcriptional transactivator and as a transcriptional repressor in the absence of thyroid hormone. Specifically, thyroid hormone receptor can repress retinoic acid-induced gene expression through interactions with retinoic acid receptor. (Retinoic acid is a potent teratogen in the frog Xenopus laevis, acting at early embryonic stages to interfere with the formation of anterior structures. Endogenous retinoic acid is thought to act in normal anterior-posterior axis formation.) We have previously shown that thyroid hormone receptor RNA (alpha isotype) is expressed and polysome-associated during Xenopus embryogenesis preceding thyroid gland maturation and endogenous thyroid hormone production (D. E. Banker, J. Bigler, and R. N. Eisenman, Mol. Cell. Biol. 11:5079-5089, 1991). To determine whether thyroid hormone receptor might influence the effects of retinoic acid in early frog development, we have examined the results of ectopic thyroid hormone receptor expression on retinoic acid teratogenesis. We demonstrate that microinjections of full-length thyroid hormone receptor RNA protect injected embryos from retinoic acid teratogenesis. DNA binding is apparently essential to this protective function, as truncated thyroid hormone receptors, lacking DNA-binding domains but including hormone-binding and dimerization domains, do not protect from retinoic acid. We have shown that microinjections of these dominant-interfering thyroid hormone receptors, as well as anti-thyroid hormone receptor antibodies, increase retinoic acid teratogenesis in injected embryos, presumably by inactivating endogenous thyroid hormone receptor. This finding suggests that endogenous thyroid hormone receptors may act to limit retinoic acid sensitivity. On the other hand, after thyroid hormone treatment, ectopic thyroid hormone receptor mediates teratogenesis that is indistinguishable from the dorsoanterior deficiencies produced in retinoic acid teratogenesis. The previously characterized retinoic acid-responsive gene, Xhox.lab2, can be induced by thyroid hormone in embryos ectopically expressing thyroid hormone receptor and is less responsive to retinoic acid in such embryos. The fact that both thyroid hormone and retinoic acid can affect overlapping gene expression pathways to produce abnormal embryonic axes and can regulate the same early-expressed gene suggests a model in which thyroid hormone receptor blocks retinoic acid receptor-mediated teratogenesis by directly repressing retinoic acid-responsive genes.
Mol Cell Biol 1993 Dec
PMID:Thyroid hormone receptor can modulate retinoic acid-mediated axis formation in frog embryogenesis. 750 77

We have previously shown that triiodothyronine (T3) regulates rat fatty acid synthesis in a tissue specific manner. Here, we determined the effects of thyroid state on mRNAs encoding the lipogenic enzymes, acetyl CoA carboxylase (ACC) and fatty acid synthase (FAS). S14 mRNA, a sequence tightly associated with lipogenesis, was also measured. Levels of the three mRNA were 9-13-fold higher in hyper- than hypothyroid liver. Limited expression in kidney and heart was also increased by thyroid hormone. In brown adipose tissue, highest levels were recorded in hypothyroid animals. Thyroid state did not affect expression in lung and brain. All these changes are consistent with those previously measured in fatty acid synthesis. In white adipose tissue, mRNA expression was increased by hyperthyroidism. This increase may not be reflected in fatty acid synthesis, since we recently showed lipogenesis to be reduced under these circumstances. All three mRNAs responded rapidly to T3 in liver, but more slowly in kidney and fat. Thus, T3 regulates lipogenesis by altering levels of ACC and FAS mRNAs. S14 mRNA changes in parallel.
Mol Cell Endocrinol 1995 Apr 28
PMID:Tissue-specific regulation of lipogenic mRNAs by thyroid hormone. 767 39


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