Academic literature on the topic 'Thyronine'
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Journal articles on the topic "Thyronine"
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Witherspoon, L. R., A. S. el Shami, S. E. Shuler, H. Neely, R. Sonnemaker, S. S. Gilbert, and K. Alyea. "Chemically blocked analog assays for free thyronines. II. Use of equilibrium dialysis to optimize the displacement by chemical blockers of T4 analog and T3 analog from albumin while avoiding displacement of T4 and T3 from thyroxin-binding globulin." Clinical Chemistry 34, no. 1 (January 1, 1988): 17–23. http://dx.doi.org/10.1093/clinchem/34.1.17.
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Abstract Chemical blockers used to displace thyronine analog from albumin in analog kits for assay of free thyroxin (FT4) or free triiodothyronine (FT3) may also displace thyroxin (T4) or triiodothyronine (T3) from thyroxin-binding globulin (TBG), resulting in an apparent TBG dependence of results of free hormone estimates. We used equilibrium dialysis and antibody binding to assess the displacement of thyronine analogs and thyronines from albumin and TBG by use of chemical blockers. We chose a combination of two chemical blockers, which eliminated thyronine analog-albumin binding but minimized thyronine displacement from TBG for use in FT4 and FT3 assays. These blocked-analog free-hormone assays yielded accurate clinical results in euthyroid patients, hypo- and hyperthyroid patients, and in pregnant women. FT4 results were not entirely normalized in all nonthyroidally ill patients, indicating that decreased analog-albumin binding is not the only factor resulting in low FT4 results. In current Diagnostic Products Corp. (DPC) FT4 and FT3 blocked-analog kits, the blocker concentrations are the same as we used in these assays.
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Zhu, Fan-Fan, and Li-Zhen Yang. "The Association Between the Levels of Thyroid Hormones and Peripheral Nerve Conduction in Patients with Type 2 Diabetes Mellitus." Experimental and Clinical Endocrinology & Diabetes 126, no. 08 (June 26, 2018): 493–504. http://dx.doi.org/10.1055/a-0635-0826.
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Abstract Background Type 2 diabetes has an underlying pathology with thyroid dysfunction. However, few studies have investigated the association between thyroid hormones and diabetic peripheral neuropathy. Our aim was to evaluate the relationship between thyroid hormones and electrophysiological properties of peripheral nerves in type 2 diabetes. Patients and Methods The medical records of 308 patients with type 2 diabetes were enrolled in this study. Subjects stratified by sex were divided into subgroups based on the diagnosis of nerve conduction study. The nerve conduction parameters were separately described with the spectrum of thyroid hormones. Multivariate regression models to analyze the potential links between thyroid hormones and nerve conduction parameters. Results The serum free triiodine thyronine levels between normal and abnormal nerve conduction groups were statistically different in total (4.55±0.65 vs 4.37±0.63, P<0.05) and female diabetic patients (4.46±0.50 vs 4.14±0.57, P<0.01). Moreover, the summed amplitude and velocity Z score of female and male increased with free triiodine thyronine levels (P<0.05). Sex-specific binary logistic regression models showed that free triiodine thyronine levels were associated with decreased odds of abnormal nerve conduction diagnosis (odds ratio [95%CI]=0.151[0.047-0.186]) and low tertile of summed amplitude Z score (odds ratio [95%CI]=0.283[0.099-0.809]) in female. In total patients, free triiodine thyronine level was negatively associated with odds of abnormal nerve conduction (odds ratio [95%CI]=0.436 [0.226-0.842]), low tertile of summed velocity (odds ratio [95%CI]=0.44[0.226-0.858]) and amplitude (odds ratio [95%CI]=0.436[0.227-0.838) Z score. Conclusions Serum free triiodine thyronine level is associated with nerve conduction in diabetes. Low free triiodine thyronine may be a potential risk for diabetic peripheral neuropathy.
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Aceves, C., and R. Rojas-Huidobro. "Effect of suckling and adrenergic stimulation on peripheral deiodination in lactating rats: differential expression of type 1 deiodinase mRNA forms." Journal of Endocrinology 171, no. 3 (December 1, 2001): 533–40. http://dx.doi.org/10.1677/joe.0.1710533.
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Previous works led us to propose that peripheral iodothyronine deiodination is mainly regulated by the reciprocal interaction between the thyroid and the sympathetic nervous system (SNS). In this study, we analyzed the role suckling exerts, through SNS activation, upon deiodination of thyronines in liver, heart, brown adipose tissue and mammary gland during lactation. Our results showed that resuckling causes a concurrent stimulatory response on deiodinase type 1 (D1) in heart and mammary gland, but not in liver and brown adipose tissue. The stimulatory response was mimicked by norepinephrine and by the beta-adrenergic agonist isoproterenol, through the overexpression of the large form of D1 mRNA. These results suggested that, during lactation, peripheral thyronine deiodination is co-ordinated by the SNS, and suckling is a major modulatory influence.
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Valashek, I. E., P. M. Kochergin, E. M. Vinogradova, and L. I. Budanova. "Synthesis of 3,5-Diiodo-DL-thyronine." Pharmaceutical Chemistry Journal 29, no. 6 (June 1995): 418–19. http://dx.doi.org/10.1007/bf02220547.
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SHOJAEE-MORADIE, Fariba, Michelle P. Y. CHAN, Micayla A. TELFER, Dietrich BRANDENBURG, Erik SUNDERMANN, Heike ECKEY, Jens KLEINJUNG, Achim SCHÜTTLER, and Richard H. JONES. "Effect of thyroid hormone binding proteins on insulin receptor binding of B1-thyronine-insulin analogues." Biochemical Journal 381, no. 1 (June 22, 2004): 51–57. http://dx.doi.org/10.1042/bj20040177.
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Certain thyronine-insulin analogues, which form non-covalent complexes with plasma proteins, have been shown to act preferentially in the liver. We hypothesized that this property may be dependant on the ability of the analogue to bind to the insulin receptor without prior dissociation from the binding protein. NαB1-L-thyroxyl-insulin, NαB1-3,3′,5′-triiodothyronine-insulin, NαB1-D-thyroxyl-insulin and NαB1-L-thyroxyl-aminolauroyl-insulin were compared with insulin for their capacity to inhibit the binding of [125I]TyrA14-insulin to rat liver plasma membrane in albumin-free buffer. Effective doses at 50% maximum inhibition of binding (ED50) were calculated with and without addition of the thyroid hormone binding proteins transthyretin, thyroxine binding globulin and human serum albumin. The binding of thyronine-insulin analogues to insulin receptors was inhibited in a dose-dependant manner by the addition of thyroid hormone binding proteins at concentrations in the physiological range. Complexes of thyronine-insulin analogues with thyroid hormone binding proteins exhibit impaired insulin receptor binding affinities compared with those of the analogues in their free form. Hepatoselectivity in vivo may not depend on binding of the intact complexes to hepatocytes. These results have implications for the physiological role of hormone binding proteins and the in vivo properties of other insulin analogues which bind to plasma proteins.
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Oziol, L., P. Faure, N. Bertrand, and P. Chomard. "Inhibition of in vitro macrophage-induced low density lipoprotein oxidation by thyroid compounds." Journal of Endocrinology 177, no. 1 (April 1, 2003): 137–46. http://dx.doi.org/10.1677/joe.0.1770137.
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Oxidized low density lipoproteins (LDL) are highly suspected of initiating the atherosclerosis process. Thyroid hormones and structural analogues have been reported to protect LDL from lipid peroxidation induced by Cu2+ or the free radical generator 2,2'-azobis-'2-amidinopropane' dihydrochloride in vitro. We have examined the effects of thyroid compounds on macrophage-induced LDL oxidation. Human monocyte-derived macrophages (differentiated U937 cells) were incubated for 24 h with LDL and different concentrations (0-20 microM) of 3,5,3'-triiodo-l -thyronine (T3), 3,5,3',5'-tetraiodo-L-thyronine (T4), 3,3',5'-tri-iodo-l -thyronine (rT3), the T3 acetic derivative (3,5,3'-tri-iodothyroacetic acid; TA3) or L-thyronine (T0) (experiment 1). Cells were also preincubated for 24 h with 1 or 10 microM of the compounds, washed twice, then incubated again for 24 h with LDL (experiment 2). Oxidation was evaluated by measurement of thiobarbituric acid-reactive substances (TBARS) and cell viability by lactate deshydrogenase release. In experiment 1, T0 had no effect, whereas the other compounds decreased LDL TBARS production, but T3 and TA3 were less active than T4 and rT3 (IC50: 11.0 +/- 2.6 and 8.1 +/- 0.8 vs 1.4 +/- 0.5 and 0.9 +/- 0.3 microM respectively). In experiment 2, the compounds at 1 microM had no effect; at 10 microM, T3 and rT3 slightly reduced LDL TBARS production, whereas TA3 and T4 inhibited it by about 50% and 70% respectively. TBARS released by the cells were also highly decreased by T3, T4, rT3 and TA3 in experiment 1, but only by T3 (30%) and T4 (70%) in experiment 2. Cell viability was not affected by the compounds except slightly by TA3 at 10 microM. The data suggested that the physico-chemical antioxidant capacity of thyroid compounds was modulated by their action on the intracellular redox systems of macrophage. Overall cellular effects of T3 led to a reduction of its antioxidant capacity whereas those of T4 increased it. Thus T4 might protect LDL against cellular oxidation in vivo more than T3.
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Segal, J., J. Hardiman, and S. H. Ingbar. "Stimulation of calcium-ATPase activity by 3,5,3′-tri-iodothyronine in rat thymocyte plasma membranes. A possible role in the modulation of cellular calcium concentration." Biochemical Journal 261, no. 3 (August 1, 1989): 749–54. http://dx.doi.org/10.1042/bj2610749.
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We have previously demonstrated that 3,5,3′-tri-iodo-L-thyronine (T3) produces a very rapid and transient increase in calcium uptake and cytoplasmic free calcium concentration in the rat thymocyte, and have postulated that Ca2+-ATPase may contribute to the overall effect of T3 on cellular calcium metabolism. In the present study, we show that in the rat thymocyte, T3 increased plasma membrane Ca2+-ATPase activity. This effect of T3 was very rapid, seen at 30 s after the addition of the hormone, and was concentration-related, evident at a physiological concentration as low as 1 pM. Evaluation of the effect of several thyronine analogues on Ca2+-ATPase activity revealed the following order of potency: D-T3 greater than or equal to 3′-isopropyl-L-T2 = L-T3 = L-T4 = D-T4 greater than L-rT3 greater than 3,5-L-T2 greater than DL-thyronine. Studies with the calmodulin antagonist trifluoperazine demonstrated that thymocyte Ca2+-ATPase activity and its stimulation by T3 are influenced by calmodulin. Other studies showed that several adrenergic agents, agonists and antagonists, had no effect on thymocyte Ca2+-ATPase activity and its stimulation by T3. From these and previous observations, we would suggest that in the rat thymocyte, the T3-induced increase in Ca2+-ATPase activity, which enhances the expulsion of calcium from the cell, plays a role in the diminution and transiency of the stimulatory effect of T3 on thymocyte calcium metabolism.
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Coppola, Maria, Federica Cioffi, Maria Moreno, Fernando Goglia, and Elena Silvestri. "3,5-diiodo-L-thyronine: A Possible Pharmacological Agent?" Current Drug Delivery 13, no. 3 (May 20, 2016): 330–38. http://dx.doi.org/10.2174/1567201813666151123124340.
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Li, Shanshan, Bing Yang, Tomonori Kobayashi, Bingchen Yu, Jun Liu, and Lei Wang. "Genetically encoding thyronine for fluorescent detection of peroxynitrite." Bioorganic & Medicinal Chemistry 28, no. 18 (September 2020): 115665. http://dx.doi.org/10.1016/j.bmc.2020.115665.
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VALASHEK, I. E., P. M. KOCHERGIN, E. M. VINOGRADOVA, and L. I. BUDANOVA. "ChemInform Abstract: Synthesis of 3,5-Diiodo-DL-thyronine." ChemInform 27, no. 2 (August 12, 2010): no. http://dx.doi.org/10.1002/chin.199602253.
Full textDissertations / Theses on the topic "Thyronine"
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Dudley, Samuel C. "The Effects of Carboxyl-group Specific Modification and Triiodo-L-thyronine on Cardiac Sodium Channels." VCU Scholars Compass, 1991. http://scholarscompass.vcu.edu/etd/4527.
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The patch clamp method was used to evaluate the effects of 3,5,3'-triiodo-L-thyronine (T3) and carboxyl modification on adult rabbit ventricular Na+ channels. In contrast to TTX-sensitive Na+ channels, Ca2+ block of cardiac Na+ channels was not prevented by selective carboxyl modification by trimethyloxonium (TMO) or water soluble carbodiimide (WSC). In 2 mM Ca2+, TMO-treated patches exhibited 3 discrete conductance (γNa) levels. An abbreviation of mean open time (MOT) accompanied each decrease in γNa. The effects on channel gating of elevating external Ca2+ differed from those of TMO pretreatment. Ensemble averages after TMO showed a shortening of the time to peak current and an acceleration of the rate of current decay. WSC caused a decrease in γNa and an abbreviation of MOT at all potentials tested. We conclude that alteration of the surface potential by a single carboxyl modification is inadequate to explain the effects of TMO and WSC. Physiological concentrations of T3 increased bursting as measured by the ratio of long events (LE) to the total number of events. In the cell-attached patch configuration, addition of 5 nM T3 to the pipette increased the %LE at all potentials examined. The increase had a biphasic voltage-dependence and peaked at -50 mV. A similar increase in the %LE occurred with 50 nM T3 suggesting saturation at ≤5 nM. LEs sometimes were grouped into runs, but the more usual pattern suggested that modal shifts occurred in ~1 s. Addition of T3 to the bath but not the pipette in cell-attached patches failed to alter the MOT, unitary current, or %LE. Na+ channel gating also was unaffected by patch excision or by addition of T3 to the cytoplasmic face of inside-out patches. Nevertheless, with T3 in the pipette, patch excision to the inside-out configuration caused a dramatic increase in the %LE, especially near the threshold potential, and an increase in the MOT. These results suggested that T3 was not membrane permeable during the time scale of the experiments and that T3's action required close proximity to the extracellular face of the Na+ channel.
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Baas, Dominique. "Action de la 3,5,3' triiodo-l-thyronine au cours du developpement de l'oligodendrocyte : etude in vitro." Strasbourg 1, 1995. http://www.theses.fr/1995STR13200.
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La triiodothyronine (t3) joue un role important lors de la maturation du systeme nerveux central chez les mammiferes. L'hypothyroidie neonatale conduit chez l'homme a un retard mental irreversible associe a un defaut de maturation des neurones des astrocytes et des oligodendrocytes (ol), induisant une hypomyelinisation et une alteration de la composition de la myeline. La t3 agit par l'intermediaire de recepteurs nucleaires specifiques (rt3) alpha et beta. La presence de rt3 dans le cerveau de rat embryonnaire et adulte a ete mise en evidence ainsi que des sites specifiques de liaison a la t3 dans les cultures d'astrocytes et d'ol. Dans ce travail, nous avons cherche a determiner l'effet de la t3 sur la differenciation des ol ainsi que sur certains genes specifiques tels que la glutamine synthetase (gs) et la proteine basique encephalitogene de la myeline (mbp) avant de determiner quel type de rt3 est exprime dans le lignage oligodendrocytaire. Une inhibition de 50% de la proliferation des precurseurs o-2a de cellules gliales ainsi qu'une ramification plus importante des ol ont ete observees apres traitement des cellules par de t3. L'arnm et la proteine de la gs sont presents dans les o-2a, les ol, les astrocytes de type-2 (a2) et les astrocytes de type-1. La t3 et l'hydrocortisone augmentent l'arnm et l'activite specifique de la gs dans les ol. Par contre, dans notre systeme de culture la t3 n'a aucun effet sur la mbp. L'arnm et la proteine du rt3alpha sont exprimes dans les precurseurs o-2a et dans les ol alors que l'arnm et la proteine du rt3betal sont exprimes uniquement dans les ol, et (pour l'arnm du rt3betal) dans les a2. La t3 stimule l'arnm du rt3betal. L'expression differencielle des rt3 suggere des fonctions specifiques de chacun d'entre eux lors de la differenciation oligodendrocytaire
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Lehmphul, Ina. "Zelluläre Wirkung, Wirkmechanismen und Nachweisverfahren von Schilddrüsenhormonen und ihren Metaboliten." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17434.
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Schilddrüsenhormone (TH) regulieren Metabolismus und Energiestoffwechsel. Der TH‐Metabolit (THM) 3,5‐T2 (3,5‐Diiod‐L‐Thyronin) aktiviert Fett‐Oxidation und mitochondriale Atmung. Der THM 3‐Iodothyronamin (3‐T1AM) beeinflusst zusätzlich glukoregulatorische Prozesse. THM können zur Reduktion von Körperfett beitragen. Um 3,5‐T2 im humanen Serum nachzuweisen sollte ein Immunoassay aufgebaut, validiert und angewendet werden. In intakten hepatozellulären (HepG2) sowie pankreatischen ß‐Zellen (MIN6) sollte untersucht werden ob THM durch Modulation der mitochondrialen Aktivität die zelluläre Substratverstoffwechslung (3,5‐T2) und Insulinsekretion (3‐T1AM) regulieren können. Der Immunoassay ist sensitiv, spezifisch und misst zuverlässig 3,5‐T2 im humanen Serum. Hyper‐ und Hypothyreose zeigen vergleichbare 3,5‐T2 Konzentrationen, jedoch akkumuliert 3,5‐T2 bei sekundären Erkrankungen der Schilddrüse und athyreoten Patienten unter Thyroxin‐Supplementation. In HepG2‐Zellen konnte die Aktivierung der mitochondrialen Atmung durch 3,3‘,5‐Triiod‐L‐Thyronin (T3), jedoch nicht durch 3,5‐T2 stimuliert werden. Die Expression von TH‐transporters (THT) war gering verglichen mit Maus‐Hepatozyten. MIN6 exprimiert THT vergleichbar mit Langerhansschen Inselzellen der Maus. 3‐T1AM wird in die Zelle aufgenommen, zu 3‐Iodothyroessigsäure (TA1) metabolisiert, und wieder exportiert. Nach 3‐T1AM Gabe ist die mitochondriale ATP‐Produktion sowie die Glukose‐stimulierte Insulinsekretion (GSIS) vermindert. 3,5‐T2 zirkuliert in euthyreoten Individuen, ist nicht an der zentralen Regulation der TH‐Achse beteiligt, wird extrathyroidal gebildet und niedrige T3‐Werte können durch erhöhtes 3,5‐T2 erklärt werden. HepG2 erwies sich als ungeeignetes Zellmodell, da wenige THT vorhanden sind, 3,5‐T2 die Plasmamembran wahrscheinlich nicht passieren kann und damit die Aktivierung der Mitochondrien aus bleibt. In MIN6 wurde gezeigt, dass die GSIS nicht ausschließlich an der Plasmamembran durch 3‐T1AM reguliert wird.Thyroid hormones (TH) regulate metabolism and energy metabolism. The TH‐metabolite (THM) 3,5‐T2 (3,5‐diiodo‐L‐thyronine) activates fat oxidation and mitochondrial respiration. The THM 3‐T1AM (3‐iodothyronamine) influences in addition glucoregulatory processes. THM may support reduction in body fat mass. It was the idea to establish, validate and apply an immunoassay to determine 3,5‐T2 in human serum. Using intact hepatocellular (HepG2) as well as pancreatic ß‐cells (MIN6) it should be tested if THM can modulate mitochondrial activity, resulting in increased cellular substrate usage (3,5‐T2) as well as decreased insulin secreation (3‐T1AM). The established immunoassay is sensitive, specific and detects precisely 3,5‐T2 in human serum. Hyper‐ and hypothyroidism shows similar 3,5‐T2 concentrations, although 3,5‐T2 accumulates in secondary thyroidal illness as well as in athyreotic patients under thyroxine‐supplementation. Using HepG2 cells, mitochondrial respiration was stimulated by 3,3‘,5‐triiodo‐L‐thyronine (T3), but 3,5‐T2 had no effect. Expression of TH‐transporters (THT) was low compared to murine hepatocytes. In contrast, MIN6 express THT comparable to murine Langerhans islets. 3‐T1AM is taken up by the cell, metabolized to 3‐iodothyroacetic acid (TA1) and following export. After 3‐T1AM application mitochondrial ATP‐production as well as glucose‐stimulated insulin secretion (GSIS) was reduced. 3,5‐T2 circulates in euthyroid individuals, is not involved in central regulation of TH‐axis, is produced extrathyroidally and low T3 values can be explained by increased 3,5‐T2. HepG2 was shown to be an inappropriate cellmodel, because THT are merely expressed, suggesting that 3,5‐T2 is not able to pass the plasma membrane, thereby preventing mitochondrial activation. In addition, it was shown in MIN6 cells, that GSIS is not exclusively regulated at the plasma membrane level via 3‐T1AM.
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Hachi, Isma. "Etude structurale de biomarqueurs de neuropathologies : cas particulier de la protéine CRYM, une Cytosolic-3,3',5-triiodo-L-thyronine(T3)-Binding Protein." Grenoble, 2010. http://www.theses.fr/2010GRENV030.
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Mon projet de thèse s'inscrit dans un vaste projet de caractérisation de protéines nouvellement identifiées dont l'expression est sélective à certaines régions du cerveau. Cette expression sélective pouvant être liée aux phénomènes de dégénérescence neuronale qui caractérisent les maladies neurodégénératives, ces protéines constituent donc des biomarqueurs potentiels. Une étude structurale et physico-chimique a été effectuée sur une dizaine de protéines, dont la protéine CRYM murine (mCRYM) qui fait parti de la famille des Cytosolic- 3,3',5-triiodo-L-thyronine(T3)-Binding Protein car elle régule la concentration en hormone thyroïdienne T3 libre dans la cellule. MCRYM appartient également à la famille des µ-crystallines et à la superfamille des µ-crystallines/Ornithines Cyclodésaminases. Les protéines présentant des homologies pour ces trois familles sont la plupart différentes par leur fonction (enzymatique ou structurale), leur localisation tissulaire et leurs caractéristiques physico-chimiques. Cette diversité est due au recrutement de gènes de la superfamille des crystallines pour diverses fonctions métaboliques tout en conservant le taxon spécifique des crystallines. Je suis parvenue à résoudre sa structure cristallographique complexée au NADP(H) et à l'hormone thyroïdienne T3 à une résolution de 1,75 Å. La protéine mCRYM est un exemple intéressant d'évolution par son appartenance à différentes familles de protéines et, à ce jour, aucune activité enzymatique n'a été identifiée. Sa caractérisation structurale et thermodynamique a donc permis de mettre en évidence les différences et les similitudes avec ses homologues enzymatiques et d'émettre des hypothèses quant à son évolution moléculaire. Ces résultats soulèvent de nouvelles questions concernant son rôle physiologique : mCRYM est-elle une enzyme ou une protéine structurale ? Comment intervient le couple redox NADPH/NADP+ pour réguler l'action génomique et/ou non génomique de l'hormone T3 ? L'hormone T3 est-il le seul ligand physiologique de CRYM dans le cerveau ?My Ph. D. Work takes part of a larger project dedicated to the characterization of proteins newly involved into selective expression of certain mouse brain regions. This selective expression being potentially linked to neuronal degeneration associated with neurodegenerative diseases, the corresponding proteins are therefore potential biomarkers. A structural and physico-chemical study has been performed on about ten proteins including CRYM of mouse (mCRYM), which belongs to the Cytosolic-3,3',5-triiodo-L-thyronine(T3)-Binding Protein family since it regulates the concentration of free thyroid hormone, T3, in the cell. MCRYM also belongs to the µ-crystallin family and to the µ-crystallins/Ornithin Cyclodesaminases superfamily. Proteins displaying sequence homologies to these three families of proteins have generally different functions (enzymatic or structural), different tissue localisation and different physico-chemical properties. This diversity is due to the recruitment of genes of the crystalline superfamily to carry different metabolic functions while preserving the taxon-specific crystallins. I have managed to resolve the crystallographic structure of mCRYM in complex with NADP(H) and the thyroid hormone, T3, to 1. 75 Å resolution. MCRYM is a very interesting evolution specimen as it belongs to a different family of proteins. However, no enzymatic function has ever been demonstrated for mCRYM. Its structural and thermodynamical characterization has revealed similitudes and divergences with the enzymatic homologues of CRYM and has allowed us to make hypothesis relative to its molecular evolution. These results raise new questions concerning the physiological role of mammalian CRYM: is CRYM an enzyme or a structural protein? How does the NADPH/NADP+ redox couple regulates the genomic and/or non genomic action of the T3 hormone? Is the T3 hormone the only physiological ligand of CRYM in the brain?
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Hachi, Isma. "Etude structurale de biomarqueurs de neuropathologies : Cas particulier de la protéine CRYM, une Cytosolic-3,3',5-triiodo-L-thyronine(T3)-Binding Protein." Phd thesis, Université de Grenoble, 2010. http://tel.archives-ouvertes.fr/tel-00718112.
Full textAbstract:
Mon projet de thèse s'inscrit dans un vaste projet de caractérisation de protéines nouvellement identifiées dont l'expression est sélective à certaines régions du cerveau. Cette expression sélective pouvant être liée aux phénomènes de dégénérescence neuronale qui caractérisent les maladies neurodégénératives, ces protéines constituent donc des biomarqueurs potentiels. Une étude structurale et physico-chimique a été effectuée sur une dizaine de protéines, dont la protéine CRYM murine (mCRYM) qui fait parti de la famille des Cytosolic- 3,3',5-triiodo-L-thyronine(T3)-Binding Protein car elle régule la concentration en hormone thyroïdienne T3 libre dans la cellule. mCRYM appartient également à la famille des µ-crystallines et à la superfamille des µ-crystallines/Ornithines Cyclodésaminases. Les protéines présentant des homologies pour ces trois familles sont la plupart différentes par leur fonction (enzymatique ou structurale), leur localisation tissulaire et leurs caractéristiques physico-chimiques. Cette diversité est due au recrutement de gènes de la superfamille des crystallines pour diverses fonctions métaboliques tout en conservant le taxon spécifique des crystallines. Je suis parvenue à résoudre sa structure cristallographique complexée au NADP(H) et à l'hormone thyroïdienne T3 à une résolution de 1,75 Å. La protéine mCRYM est un exemple intéressant d'évolution par son appartenance à différentes familles de protéines et, à ce jour, aucune activité enzymatique n'a été identifiée. Sa caractérisation structurale et thermodynamique a donc permis de mettre en évidence les différences et les similitudes avec ses homologues enzymatiques et d'émettre des hypothèses quant à son évolution moléculaire. Ces résultats soulèvent de nouvelles questions concernant son rôle physiologique : mCRYM est-elle une enzyme ou une protéine structurale ? Comment intervient le couple redox NADPH/NADP+ pour réguler l'action génomique et/ou non génomique de l'hormone T3 ? L'hormone T3 est-il le seul ligand physiologique de CRYM dans le cerveau ?
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Gonzales, Christopher R. "3,3′,5′-triido-L-thyronine alters protein kinase B, phosphotase and tensin homolog and connective tissue growth factor expression in human dermal fibroblasts." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12397.
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Thesis (M.A.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.Cutaneous tissue repair is complex and involves a variety of growth factors to regulate a balance of regeneration and fibrosis during healing. This process is divided into three sequential and overlapping phases: the inflammatory phase, the proliferative phase, and the remodeling phase. Fibroblasts are crucial during this process in that they help initiate inflammatory activity, deposit extracellular matrix proteins for granulation tissue and deconstruct granulation tissue to make way for mature scar formation. Previous studies on the effects of 3,3',5'-triiodo-L-thyronine (T3) on skin have revealed that healing tissue responds to T3 by accelerating skin cell proliferation and migration. These findings indicate that T3 offers potential as a therapeutic drug for individuals with extensive cutaneous damage, chronic skin maladies or retarded wound healing. The mechanisms underlying these changes are not clearly understood, however, elucidation of changes in protein expression patterns should be evaluated to appropriately judge the therapeutic potential of T3. This study aims to characterize T3 dose responsive expression of protein kinase B, phosphatase and tensin homolog, connective tissue growth factor and wnt5a. Western blot analysis and immunodetection revealed that wnt5a is not expressed in human dermal fibroblasts. Protein kinase B did not vary significantly with T3 concentration ranging from 1.0 nM-1.0 1µM, F(4,5)= 1.93, p > 0.05, nor did connective tissue growth factor, F(4,5) = 2.16, p > 0.05. In contrast, phosphatase and tensin homolog showed a statistically significant change in expression, F(4, 15) = 4.67, p less than 0.05. The results presented here provide insight into protein pathways and growth factors through which thyroid hormone produces its effects on the various cells of the integument and suggests that phosphatase and tensin homolog (PTEN) expression levels are responsive to varying concentrations of T3. Future studies should further evaluate the role of T3 on its various targets as a therapeutic option for skin disorders.
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Serrar, Mostafa. "Effets croisés des régimes enrichis en stérols ou en acides biliaires et du traitement par la 3, 5,3’triiodo-L-thyronine (t3) sur les activités des enzymes microsomales hépatiques responsables du métabolisme des xénobiotiques chez le rat." Dijon, 1987. http://www.theses.fr/1987DIJOS043.
Full textAbstract:
La supplémentation des régimes alimentaires en stérols ou en acide biliaire provoque une augmentation du taux de cholestérol et de phospholipides dans les microsomes hépatiques et une diminution du taux de malandialdéhyde. L’administration de T3 provoque l'effet inverse
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Nicolas, Patrick. "Modulation pharmacologique des activités thyronine-désiodases, enzymes de monodésiodation des hormones thyroi͏̈diennes : application : la 5'-désiodase de type II (5D'II) et la triiodothyronine (T) dans la correction des troubles de l'humeur." Paris 13, 1996. http://www.theses.fr/1996PA1300T1.
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Les iodothyronine-désiodases sont des sélénoprotéines qui catalysent les réactions de monodésiodation des hormones thyroi͏̈diennes (HT). Trois enzymes différentes sont actuellement clonées. La 5'-désiodase de type I (5'DI) et la 5-désiodase de type III (5DIII) réalisent plutôt une inactivation du système thyroi͏̈dien tandis que la 5'-désiodase de type II (5'DII) active ce système en désiodant la thyroxine (T4) inactive en triiodothyronine (T3) active. En l'absence de substances capables de mimer ou au contraire de s'opposer aux effets de la T3 sur son récepteur nucléaire, la modulation pharmacologique des iodothyronine-désiodases constitue une façon indirecte de parvenir aux mêmes résultats. Nous avons alors étudié l'effet de 5 macrolides sur la 5'DI hépatique. Chez le rat, l'erythromycine, la josamycine et la troléandomycine inhibent la 5'DI, alors que la midécamycine et la spiramycine sont sans effet. Chez l'homme, la troléandomycine provoque des anomlies du bilan thyroi͏̈dien éventuellem̀ent liées à une inhibition de la 5'DI hépatique tandis que la josamycine rest sans effet. Ces deux études rapportent pour la première fois des effets inhibiteurs de certains macrolides sur la 5'DI et fournissent des éléments qui permettent d'écarter tout lien entre 5'DI et mono-oxygénases mixtes à cytochrome P-450. Les effets de l'amiodarone ont également été étudiés sur les 3 iodothyronine-désiodases. Nous confirmons que l'amiodarone est un puissant inhibiteur de la 5'DI tout en précisant le mécanisme de cet effet inhibiteur. Nous montrons en revanche que l'amiodarone est sans effet sur la 5'DII et la 5DIII. Le rôle des HT dans les troubles de l'humeur est connu depuis longtemps et l'addition de T3 aux médicaments antidépresseurs paraît améliorer la réponse thérapeutique chez certains patients déprimés. Aussi, nous avons exploré les effets du statut thyroi͏̈dien chez l'animal et sur des astrocytes en culture primaire, en mesurant la densité des récepteurs ß-adrénergiques du cortex et du cervelet, dans le cadre de la théorie monominergique de la dépression. . .
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Piehl, Susanne. "The roles of deiodinases in thyronamine biology." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15795.
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3-Jodthyronamin (3-T1AM) und Thyronamin (T0AM) sind endogene Signalmoleküle, die eine große strukturelle Ähnlichkeit zu Schilddrüsenhormonen aufweisen, allerdings die klassischen Wirkungen des aktiven Schilddrüsenhormons 3,5,3’-Trijodthyronin (T3) antagonisieren. In der vorliegenden Arbeit wurde untersucht, ob Thyronamine (TAMs) Substrate von Dejodasen (Dio1, Dio2, Dio3) sind. Die TAMs wurden mit isozymspezifischen Dio-Präparationen inkubiert. Die Dejodierungsprodukte wurden mittels Hochleistungsflüssigkeitschromatographie und Tandemmassenspektrometrie (LC-MS/MS) analysiert. Mit Präparationen der Dio1 wurden Dejodierungen von 3,3’,5’-Trijodthyronamin, 3’,5’- und 3,3’-Dijodthyronamin am phenolischen Ring sowie Dejodierungen von 3,5,3’-Trijodthyronamin und 3,5-Dijodthyronamin am Tyrosylring beobachtet. Dio2 haltige Präparationen katalysierten ebenfalls Dejodierungen von 3,3’,5’-Trijodthyronamin und 3’,5’-Dijodthyronamin am phenolischen Ring. Mit Dio3 haltigen Präparationen wurden alle TAMs mit jodiertem Tyrosylring dejodiert. In Kompetitionsversuchen inhibierten ausschließlich die TAMs, die als Substrate von Dio Isozymen identifizierten wurden, eine etablierte Dejodierungsreaktion eines bekannten Substrats. Im Gegensatz dazu interferierten TAMs, die in den LC-MS/MS Experimenten als Substrate der Dio Isozyme ausgeschlossen wurden, nicht mit der genannten etablierten Dejodierungsreaktion. Zusammenfassend wurde in der vorliegenden Arbeit gezeigt, dass TAMs Substrate aller drei Dio Isozyme sind und jedes Isozym eine eigene Substratspezifität aufweist. Diese Befunde weisen darauf hin, dass Dio Isozyme an der Biosynthese von TAMs beteiligt sein könnten. Ferner wurden die Biosynthesewege für 3-T1AM und T0AM eingegrenzt. Desweiteren gestatten die Ergebnisse neue Einblicke in die generellen strukturellen Voraussetzungen für Dio Substrate, da TAMs die bisher einzigen endogenen Dio Substrate darstellen, deren Seitenkette am Tyrosylring eine positive Ladung aufweist.3-iodothyronamine (3-T1AM) and thyronamine (T0AM) are novel endogenous signaling molecules that exhibit great structural similarity to thyroid hormones but apparently antagonize classical thyroid hormone (T3) actions. The present study investigated whether thyronamines (TAMs) are substrates of three Dio isozymes (Dio1, Dio2 and Dio3). TAMs were incubated with isozyme specific Dio preparations. Deiodination products were analyzed using a newly established method applying liquid chromatography and tandem mass spectrometry (LC-MS/MS). Phenolic ring deiodinations of 3,3’,5’-triiodothyronamine, 3’,5’- and 3,3’-diiodothyronamine as well as tyrosyl ring deiodinations of 3,5,3’-triiodothyronamine and 3,5-diiodothyronamine were observed with preparations containing Dio1. Preparations of Dio2 also deiodinated 3,3’,5’-triiodothyronamine and 3’,5’-diiodothyronamine at the phenolic rings. All TAMs with tyrosyl ring iodine atoms were deiodinated by Dio3 containing preparations. In functional competition assays, the newly identified TAM substrates inhibited an established iodothyronine deiodination reaction. By contrast, TAMs which had been excluded as Dio substrates in LC-MS/MS experiments, failed to show any effect in the competition assays, thus verifying the former results. In summary, all three Dio isozymes catalyzed TAM deiodination reactions with each isozyme exhibiting a unique substrate specificity. These data support a role for Dio isozymes in TAM biosynthesis and contribute to confining the biosynthetic pathways of 3-T1AM and T0AM. Furthermore, they provide new insights into the structural requirements for Dio substrates in general since TAMs represent the only endogenous Dio substrates described, so far, which possess a positively charged tyrosyl ring side chain.
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Hanna, Atef Nagib. "Inhibition of low density lipoprotein oxidation by thyronines, probucol, ascorbate and ACI-reductones /." The Ohio State University, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487843314697076.
Full textBook chapters on the topic "Thyronine"
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Lissitzky, S., and S. Bouchilloux. "Enzymic Aspects of Thyronine Metabolism and its Iodinated Derivatives." In Ciba Foundation Symposium - Regulation and Mode of Action of Thyroid Hormones (Colloquia on Endocrinology, Vol. 10), 135–55. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719022.ch10.
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Roche, Jean, Raymond Michel, and Pierre Jouan. "On the Presence of 3:5:3′-Triiodothyro-Acetic Acid and 3:3′-Diiodothyronine in Rat Muscle and Kidney after Administration of 3:5:3′-Triiodo-L-Thyronine." In Ciba Foundation Symposium - Regulation and Mode of Action of Thyroid Hormones (Colloquia on Endocrinology, Vol. 10), 168–81. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719022.ch12.
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"Thyronine (3p-[p(p-hydroxyphenoxy)-phenyl]-l-alanine)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1966. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_16982.
Full textConference papers on the topic "Thyronine"
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Lei, Jianxun, Douglas O. Wangensteen, and David H. Ingbar. "3,3',5-Triiodo-L-Thyronine (T3) Enhances Adult Alveolar Type II Cell Survival Under Hyperoxia." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1965.
Full textReports on the topic "Thyronine"
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Wahl, Troy. Developing Thyronamine Analog Pharmaceuticals Targeting TAAR1 to Treat Methamphetamine Addiction. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1109.
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