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[PMID]:28938413
[Au] Autor:Pappa T; Anselmo J; Mamanasiri S; Dumitrescu AM; Weiss RE; Refetoff S
[Ad] Endereço:Departments of Medicine, The University of Chicago, Chicago, Illinois 60637.
[Ti] Título:Prenatal Diagnosis of Resistance to Thyroid Hormone and Its Clinical Implications.
[So] Source:J Clin Endocrinol Metab;102(10):3775-3782, 2017 Oct 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Resistance to thyroid hormone-ß (RTH-ß) is an autosomal dominant disorder characterized by reduced sensitivity of target tissues to thyroid hormones (THs). Individuals with RTH-ß have high TH levels usually due to mutations in the TH receptor-ß (THRB) gene. The management of RTH-ß during pregnancy is challenging, as wild-type (WT) fetuses born to RTH-ß mothers have low birth weight and suppressed postnatal thyroid-stimulating hormone (TSH), due to intrauterine exposure to excess TH. Objective: To determine birth weight and postnatal TSH of WT fetuses carried by mothers with RTH-ß whose fT4 levels were maintained below 20% of the upper limit of normal (ULN). Design: Retrospective chart review. Setting: Academic institution in collaboration with off-site hospitals and private practices. Patients: Thirteen women harboring THRB gene mutations were evaluated during 18 pregnancies. Intervention: Prenatal genetic diagnosis by amniocentesis. Women carrying WT fetuses were given the option of treatment with antithyroid medication by their treating physicians with the aim to avoid serum fT4 levels above 20% of the ULN. Results: No significant difference was found in birth weight corrected for gestational age and in serum TSH levels at birth between WT and RTH-ß infants born to RTH-ß mothers. Conclusions: Prenatal diagnosis may play an important role in the management of RTH-ß during pregnancy. Aiming for maternal fT4 levels not above 50% of the ULN in RTH-ß mothers carrying WT fetuses seems to be a prudent approach that prevents the otherwise expected low birth weight and postnatal TSH suppression.
[Mh] Termos MeSH primário: Complicações na Gravidez/diagnóstico
Complicações na Gravidez/epidemiologia
Resultado da Gravidez/epidemiologia
Diagnóstico Pré-Natal
Síndrome da Resistência aos Hormônios Tireóideos/diagnóstico
Síndrome da Resistência aos Hormônios Tireóideos/epidemiologia
[Mh] Termos MeSH secundário: Adulto
Substituição de Aminoácidos
Peso ao Nascer
Feminino
Genótipo
Seres Humanos
Masculino
Mães
Mutação de Sentido Incorreto
Gravidez
Complicações na Gravidez/genética
Diagnóstico Pré-Natal/estatística & dados numéricos
Prognóstico
Estudos Retrospectivos
Receptores beta dos Hormônios Tireóideos/genética
Síndrome da Resistência aos Hormônios Tireóideos/genética
Hormônios Tireóideos/sangue
Tireotropina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors beta); 0 (Thyroid Hormones); 9002-71-5 (Thyrotropin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-01251


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[PMID]:28443527
[Au] Autor:McGovern FM; Sweeney T; Ryan MT; Lott S; Campion FP; Boland TM
[Ad] Endereço:1School of Agriculture and Food Science,Lyons Research Farm,University College Dublin (UCD),Newcastle,Co. Kildare,W23 ENY2,Republic of Ireland.
[Ti] Título:An investigation into the effects of maternal supplementation with excess iodine on the mechanisms and impacts of reduced IgG absorption in the lamb postpartum.
[So] Source:Br J Nutr;117(7):951-963, 2017 Apr.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:An experiment was conducted to determine: (1) the effect of excess maternal I supplementation on the thyroid hormone status of the ewe and her progeny; (2) potential mechanisms underpinning the failure of passive transfer associated with excess I and (3) the growing lambs' response to natural gastrointestinal infection. Twin-bearing ewes received one of two treatments (n 32/treatment group): basal diet (C) or C plus 26·6 mg of iodine/ewe per d (I), supplied as calcium iodate. Ewes were individually fed from day 119 of gestation to parturition. Progeny of I ewes had lower (P<0·01) serum IgG concentrations from 24 h to 28 d postpartum but higher serum IgG concentrations at day 70 postpartum (P<0·05). I supplementation increased the relative expression of Fc receptor, IgA, IgM high affinity and polymeric Ig receptor in the ileum of the lamb at 24 h postpartum; however, thyroid hormone receptor-ß (THRB) and ß-2-microglobulin (B2M) expression declined (P<0·05). Progeny of I ewes had higher growth rates to weaning (P<0·05) and lower faecal egg count (FEC) for Nematodirus battus (P<0·05) between weeks 6 and 10 postpartum. In conclusion, excess maternal I supplementation negatively affected the thyroid hormone status, serum IgG concentration, ileal morphology and the gene expression of THRB and B2M in the ileum and ras-related protein (RAB) RAB25 and the mucin gene (MUC) MUC1 in the duodenum of the lamb postpartum. These effects were followed by an enhancement of average daily gain and lower N. battus FEC in the pre-weaning period of I-supplemented lambs.
[Mh] Termos MeSH primário: Colostro/imunologia
Suplementos Nutricionais
Imunidade Materno-Adquirida
Iodo/uso terapêutico
Fenômenos Fisiológicos da Nutrição Materna
Doenças dos Ovinos/prevenção & controle
Infecções por Strongylida/veterinária
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Colostro/química
Suplementos Nutricionais/efeitos adversos
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Íleo/crescimento & desenvolvimento
Íleo/imunologia
Íleo/metabolismo
Íleo/patologia
Imunoglobulina G/análise
Imunoglobulina G/biossíntese
Mucosa Intestinal/crescimento & desenvolvimento
Mucosa Intestinal/imunologia
Mucosa Intestinal/metabolismo
Mucosa Intestinal/patologia
Iodo/efeitos adversos
Masculino
Nematodirus/imunologia
Nematodirus/isolamento & purificação
Contagem de Ovos de Parasitas/veterinária
Gravidez
Distribuição Aleatória
Ovinos
Doenças dos Ovinos/imunologia
Doenças dos Ovinos/metabolismo
Doenças dos Ovinos/parasitologia
Carneiro Doméstico
Infecções por Strongylida/imunologia
Infecções por Strongylida/parasitologia
Infecções por Strongylida/prevenção & controle
Receptores beta dos Hormônios Tireóideos/genética
Receptores beta dos Hormônios Tireóideos/metabolismo
Ganho de Peso
Microglobulina-2 beta/genética
Microglobulina-2 beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin G); 0 (Thyroid Hormone Receptors beta); 0 (beta 2-Microglobulin); 9679TC07X4 (Iodine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517000575


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[PMID]:28300834
[Au] Autor:Fulton J; Mazumder B; Whitchurch JB; Monteiro CJ; Collins HM; Chan CM; Clemente MP; Hernandez-Quiles M; Stewart EA; Amoaku WM; Moran PM; Mongan NP; Persson JL; Ali S; Heery DM
[Ad] Endereço:School of Pharmacy, University of Nottingham, Nottingham, UK.
[Ti] Título:Heterodimers of photoreceptor-specific nuclear receptor (PNR/NR2E3) and peroxisome proliferator-activated receptor-γ (PPARγ) are disrupted by retinal disease-associated mutations.
[So] Source:Cell Death Dis;8(3):e2677, 2017 Mar 16.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Photoreceptor-specific nuclear receptor (PNR/NR2E3) and Tailless homolog (TLX/NR2E1) are human orthologs of the NR2E group, a subgroup of phylogenetically related members of the nuclear receptor (NR) superfamily of transcription factors. We assessed the ability of these NRs to form heterodimers with other members of the human NRs representing all major subgroups. The TLX ligand-binding domain (LBD) did not appear to form homodimers or interact directly with any other NR tested. The PNR LBD was able to form homodimers, but also exhibited robust interactions with the LBDs of peroxisome proliferator-activated receptor-γ (PPARγ)/NR1C3 and thyroid hormone receptor b (TRb) TRß/NR1A2. The binding of PNR to PPARγ was specific for this paralog, as no interaction was observed with the LBDs of PPARα/NR1C1 or PPARδ/NR1C2. In support of these findings, PPARγ and PNR were found to be co-expressed in human retinal tissue extracts and could be co-immunoprecipitated as a native complex. Selected sequence variants in the PNR LBD associated with human retinopathies, or a mutation in the dimerization region of PPARγ LBD associated with familial partial lipodystrophy type 3, were found to disrupt PNR/PPARγ complex formation. Wild-type PNR, but not a PNR309G mutant, was able to repress PPARγ-mediated transcription in reporter assays. In summary, our results reveal novel heterodimer interactions in the NR superfamily, suggesting previously unknown functional interactions of PNR with PPARγ and TRß that have potential importance in retinal development and disease.
[Mh] Termos MeSH primário: Mutação/genética
Receptores Nucleares Órfãos/genética
PPAR gama/genética
Retina/patologia
Doenças Retinianas/genética
Doenças Retinianas/patologia
[Mh] Termos MeSH secundário: Linhagem Celular
Linhagem Celular Tumoral
Dimerização
Células HEK293
Seres Humanos
Membro 1 do Grupo D da Subfamília 1 de Receptores Nucleares/genética
Conformação Proteica
Receptores beta dos Hormônios Tireóideos/genética
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NR2E3 protein, human); 0 (Nuclear Receptor Subfamily 1, Group D, Member 1); 0 (Orphan Nuclear Receptors); 0 (PPAR gamma); 0 (Thyroid Hormone Receptors beta); 0 (Transcription Factors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2017.98


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[PMID]:28229360
[Au] Autor:Lindsey RC; Mohan S
[Ad] Endereço:Musculoskeletal Disease Center, VA Loma Linda Healthcare System, Loma Linda, CA, USA.
[Ti] Título:Thyroid hormone acting via TRß induces expression of browning genes in mouse bone marrow adipose tissue.
[So] Source:Endocrine;56(1):109-120, 2017 Apr.
[Is] ISSN:1559-0100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Mutant hypothyroid mouse models have recently shown that thyroid hormone is critical for skeletal development during an important prepubertal growth period. Additionally, thyroid hormone negatively regulates total body fat, consistent with the well-established effects of thyroid hormone on energy and fat metabolism. Since bone marrow mesenchymal stromal cells differentiate into both adipocytes and osteoblasts and a relationship between bone marrow adipogenesis and osteogenesis has been predicted, we hypothesized thyroid hormone deficiency during the postnatal growth period increases marrow adiposity in mice. METHODS: Marrow adiposity in TH-deficient (Tshr ) mice treated with T3/T4, TH receptor ß-specific agonist GC-1, or vehicle control was evaluated via dual-energy X-ray absorptiometry and osmium micro-computed tomography. To further examine the mechanism for thyroid hormone regulation of marrow adiposity, we used real-time RT-PCR to measure the effects of thyroid hormone on adipocyte differentiation markers in primary mouse bone marrow mesenchymal stromal cells and two mouse cell lines in vitro and in Tshr mice in vivo. RESULTS: Marrow adiposity increased >20% (P < 0.01) in Tshr mice at 3 weeks of age, and treatment with T3/T4 when serum thyroid hormone normally increases (day 5-14) rescued this phenotype. Furthermore, GC-1 rescued this phenotype equally well, suggesting this thyroid hormone effect is in part mediated via TRß signaling. Treatment of bone marrow mesenchymal stromal or ST2 cells with T3 or GC-1 significantly increased expression of several brown/beige fat markers. Moreover, injection of T3/T4 increased browning-specific markers in white fat of Tshr mice. CONCLUSIONS: These data suggest that thyroid hormone regulation of marrow adiposity is mediated at least in part via activation of TRß signaling.
[Mh] Termos MeSH primário: Tecido Adiposo/metabolismo
Medula Óssea/metabolismo
Receptores da Tireotropina/metabolismo
Receptores beta dos Hormônios Tireóideos/metabolismo
Tiroxina/farmacologia
Tri-Iodotironina/farmacologia
[Mh] Termos MeSH secundário: Acetatos/farmacologia
Adipogenia/efeitos dos fármacos
Adipogenia/fisiologia
Tecido Adiposo/efeitos dos fármacos
Animais
Medula Óssea/efeitos dos fármacos
Linhagem Celular
Camundongos
Camundongos Knockout
Fenóis/farmacologia
Receptores da Tireotropina/genética
Receptores beta dos Hormônios Tireóideos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetates); 0 (GC 1 compound); 0 (Phenols); 0 (Receptors, Thyrotropin); 0 (Thyroid Hormone Receptors beta); 06LU7C9H1V (Triiodothyronine); Q51BO43MG4 (Thyroxine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170224
[St] Status:MEDLINE
[do] DOI:10.1007/s12020-017-1265-x


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[PMID]:28053002
[Au] Autor:Hernández-Puga G; Mendoza A; León-Del-Río A; Orozco A
[Ad] Endereço:Departamento de Neurobiología Celular y MolecularInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, Mexico.
[Ti] Título:Jab1 is a T2-dependent coactivator or a T3-dependent corepressor of TRB1-mediated gene regulation.
[So] Source:J Endocrinol;232(3):451-459, 2017 Mar.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Thyroid hormones (THs) induce pleiotropic effects in vertebrates, mainly through the activation or repression of gene expression. These mechanisms involve thyroid hormone binding to thyroid hormone receptors, an event that is followed by the sequential recruitment of coactivator or corepressor proteins, which in turn modify the rate of transcription. In the present study, we looked for specific coregulators recruited by the long isoform of the teleostean thyroid hormone receptor beta 1 (L-Trb1) when bound to the bioactive TH, 3,5-T (T ). We found that jun activation domain-binding protein1 (Jab1) interacts with L-Trb1 + T complex. Using both the teleostean and human TRB1 isoforms, we characterized the Jab1-TRB1 by yeast two-hybrid, pull-down and transactivation assays. Our results showed that the TRB1-Jab1 interaction was ligand dependent and involved the single Jab1 nuclear receptor box, as well as the ligand-binding and N-terminal domains of TRB1. We also provide evidence of ligand-dependent, dual coregulatory properties of Jab1. Indeed, when T is bound to L-Trb1 or hTRB1, Jab1 acts as a coactivator of transcription, whereas it has corepressor activity when interacting with the T -bound S-Trb1 or hTRB1. These mechanisms could explain some of the pleiotropic actions exerted by THs to regulate diverse biological processes.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas/metabolismo
Receptores beta dos Hormônios Tireóideos/metabolismo
Hormônios Tireóideos/farmacologia
[Mh] Termos MeSH secundário: Animais
Complexo do Signalossomo COP9
Linhagem Celular
Relação Dose-Resposta a Droga
Peptídeos e Proteínas de Sinalização Intracelular
Proteínas/genética
Ratos
Receptores dos Hormônios Tireóideos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gps1 protein, rat); 0 (Intracellular Signaling Peptides and Proteins); 0 (Proteins); 0 (Receptors, Thyroid Hormone); 0 (Thyroid Hormone Receptors beta); 0 (Thyroid Hormones); EC 3.4.19.12 (COP9 Signalosome Complex)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-16-0485


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[PMID]:27734462
[Au] Autor:Li Y; Zhang Q; Du Z; Lu Z; Liu S; Zhang L; Ding N; Bao B; Yang Y; Xiong Q; Wang H; Zhang Z; Qu H; Jia H; Fang X
[Ad] Endereço:CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, China.
[Ti] Título:MicroRNA 200a inhibits erythroid differentiation by targeting PDCD4 and THRB.
[So] Source:Br J Haematol;176(1):50-64, 2017 Jan.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Previous studies on erythropoiesis revealed that microRNAs (miRNAs) play a critical role in erythroid differentiation. Given the abundance of identified miRNAs and the limited understanding of erythroid miRNAs, additional examination is required. Here, two sets of erythroid differentiation miRNome data were analysed to screen for novel erythroid-inhibiting miRNAs. MIR200A was selected based on its pattern of downregulated expression in the miRNome datasets during induction of erythroid differentiation. Overexpression of MIR200A in K562 and TF-1 cells confirmed its inhibitory role in erythroid differentiation. Further in vivo study indicated that overexpression of mir200a inhibited primitive erythropoiesis of zebrafish. Transcriptome analyses after MIR200A overexpression in TF-1 cells indicated a significant role in regulating erythroid function and revealed potential regulation networks. Additionally, bioinformatics and experimental analyses confirmed that PDCD4 (programmed cell death 4) and THRB (thyroid hormone receptor, beta) are both targets of MIR200A-3p. Gain- and loss-of-function studies of PDCD4 and THRB revealed that the two targets were capable of promoting erythroid gene expression. Overall, our results revealed that microRNA 200a inhibits erythroid differentiation by targeting PDCD4 and THRB.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/antagonistas & inibidores
Diferenciação Celular
Células Eritroides/citologia
MicroRNAs/genética
Proteínas de Ligação a RNA/antagonistas & inibidores
Receptores beta dos Hormônios Tireóideos/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Eritropoese/genética
Seres Humanos
Células K562
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (MIRN200 microRNA, human); 0 (MicroRNAs); 0 (PDCD4 protein, human); 0 (RNA-Binding Proteins); 0 (Thyroid Hormone Receptors beta)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170518
[Lr] Data última revisão:
170518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161014
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14377


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[PMID]:27254276
[Au] Autor:Park JW; Zhao L; Willingham MC; Cheng SY
[Ad] Endereço:Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
[Ti] Título:Loss of tyrosine phosphorylation at Y406 abrogates the tumor suppressor functions of the thyroid hormone receptor ß.
[So] Source:Mol Carcinog;56(2):489-498, 2017 Feb.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have recently identified that phosphorylation at tyrosine (Y)406 is critical for the tumor suppressor functions of the thyroid hormone receptor ß1 (TRß) in a breast cancer line. However, still unclear is whether the critical tumor suppressor role of phosphorylated Y406 of TRß is limited to only breast cancer cells or could be extended to other cell types. In the present studies, we addressed this question by stably expressing TRß, a mutated TRß oncogene (PV), or a TRß mutated at Y406 (TRßY406F) in rat PCCL3 thyroid follicular cells and evaluated their tumor characteristics in athymic mice with elevated thyroid stimulating hormone. PCCL3 cells stably expressing PV (PCCL3-PV), TRßY406F (PCCL3-TRßY406F), or vector only (PCCL3-Neo) developed tumors with sizes in the rank order of TRßY406F>PV = Neo, whereas PCCL3 cells expressing TRß (PCCL3-TRß) barely developed tumors. As evidenced by markedly elevated Ki67, cyclin D1, and p-Rb protein abundance, proliferative activity was high in PV and TRßY406F tumors, but low in TRß tumors. These results indicate that TRß acted as a tumor suppressor in PCCL3 cells, whereas TRßY406F and PV had lost tumor suppressor activity. Interestingly, TRßY406F tumors had very low necrotic areas with decreased TNFα-NFκB signaling to lower apoptotic activity. In contrast, PV tumors had prominent large necrotic areas, with no apparent changes in TNFα-NFκB signaling, indicating distinct oncogenic activities of mutant PV and TRßY406F. Thus, the present studies uncovered a novel mechanism by which TRß could function as a tumor suppressor through modulation of the TNFα-NFκB signaling. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Mutação Puntual
Glândula Tireoide/patologia
Receptores beta dos Hormônios Tireóideos/genética
Neoplasias da Glândula Tireoide/genética
Neoplasias da Glândula Tireoide/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Linhagem Celular Tumoral
Proliferação Celular
Feminino
Genes Supressores de Tumor
Seres Humanos
Camundongos
Camundongos Nus
Fosforilação
Ratos
Glândula Tireoide/metabolismo
Receptores beta dos Hormônios Tireóideos/química
Tirosina/análise
Tirosina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors beta); 42HK56048U (Tyrosine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160603
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22511


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[PMID]:28222413
[Au] Autor:Neamtu C; Tupea C; Paun D; Hoisescu A; Ghemigian A; Refetoff S; Sriphrapradang C
[Ad] Endereço:National Institute of Endocrinology "C.I. Parhon", Bucharest, Romania.
[Ti] Título:A new TRß mutation in resistance to thyroid hormone syndrome.
[So] Source:Hormones (Athens);15(4):534-539, 2016 Oct.
[Is] ISSN:1109-3099
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Thyroid hormones (TH) exert their actions by binding nuclear receptors alpha (TRα1) and beta (TRß1 and TRß2). Resistance to thyroid hormone (RTH) is a clinical syndrome with various clinical manifestations, its hallmark being decreased tissue sensitivity to the action of thyroid hormones. We report the case of a family harbouring a novel TRß mutation. Sequencing of the TRß gene revealed a single nucleotide substitution-C to G in codon 340: glutamine was replaced by glutamic acid. The clinical picture and biochemical and hormonal panel showed significant differences within the family, despite their sharing the same mutation. We also present the result of low-dose antithyroid treatment in one member of the family diagnosed with this rare condition.
[Mh] Termos MeSH primário: Receptores beta dos Hormônios Tireóideos/genética
Síndrome da Resistência aos Hormônios Tireóideos/sangue
Síndrome da Resistência aos Hormônios Tireóideos/genética
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Mutação
Linhagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors beta)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.14310/horm.2002.1700


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[PMID]:27980311
[Au] Autor:Kurozumi A; Okada Y; Arao T; Tanaka Y
[Ad] Endereço:First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan.
[Ti] Título:A Case of Resistance to Thyroid Hormone (RTH) with a Negative Family History with Diagnosis Based on Persistent Palpitations.
[So] Source:J UOEH;38(4):291-296, 2016.
[Is] ISSN:0387-821X
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Approximately 140 different mutations of thyroid hormone receptor ß (TRß) have been identified in resistance to thyroid hormone (RTH). We report herein a middle-aged man with a negative family history who was diagnosed with RTH based on persistent palpitations. Genetic analysis showed a TRß mutation causing the substitution of alanine for proline 453 (P453A) in exon 10. Since treatment of RTH is different from that of Graves' disease and thyroid stimulating hormone-producing adenoma (TSHoma), a genetic analysis should be performed even in patients who have a negative family history of RTH and who are free of TSHoma when they present with persistent inappropriate secretion of thyroid stimulating hormone (SITSH).
[Mh] Termos MeSH primário: Síndrome da Resistência aos Hormônios Tireóideos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Sequência de Bases
Feminino
Seres Humanos
Masculino
Meia-Idade
Mutação
Receptores beta dos Hormônios Tireóideos/genética
Síndrome da Resistência aos Hormônios Tireóideos/genética
Tireotropina/farmacologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thyroid Hormone Receptors beta); 9002-71-5 (Thyrotropin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


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[PMID]:27853072
[Au] Autor:Wakasaki H; Matsumoto M; Tamaki S; Miyata K; Yamamoto S; Minaga T; Hayashi Y; Komukai K; Imanishi T; Yamaoka H; Matsuno S; Nishi M; Akamizu T
[Ad] Endereço:Department of Endocrinology and Diabetology, Hidaka General Hospital, Japan.
[Ti] Título:Resistance to Thyroid Hormone Complicated with Type 2 Diabetes and Cardiomyopathy in a Patient with a TRß Mutation.
[So] Source:Intern Med;55(22):3295-3299, 2016.
[Is] ISSN:1349-7235
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Resistance to thyroid hormone (RTH) is a genetic disorder characterized by reduced tissue responsiveness to thyroid hormone. We herein describe a 60-year old man who presented with the clinical features of cardiomyopathy, diabetes mellitus and elevated thyroid hormones with unsuppressed thyroid stimulating hormone. A genetic analysis of thyroid hormone receptor (TR) revealed a missense mutation (A268D) in the TRß gene. Clinical manifestations of RTH may be variable due to different tissue distributions of TR subtypes and different actions of mutant receptors. The current case demonstrates that patients with a TRß mutation may have impaired his glucose metabolism and a reduced cardiac function, although patients appear clinically euthyroid.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/complicações
Cardiomiopatias Diabéticas/complicações
Insuficiência Cardíaca/complicações
Receptores beta dos Hormônios Tireóideos/genética
Síndrome da Resistência aos Hormônios Tireóideos/complicações
Síndrome da Resistência aos Hormônios Tireóideos/genética
[Mh] Termos MeSH secundário: Diabetes Mellitus Tipo 2/sangue
Seres Humanos
Masculino
Meia-Idade
Mutação de Sentido Incorreto
Receptores dos Hormônios Tireóideos/sangue
Tireotropina/sangue
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Thyroid Hormone); 0 (Thyroid Hormone Receptors beta); 9002-71-5 (Thyrotropin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161118
[St] Status:MEDLINE



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