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Data suggest that gestational/maternal endocrine disruptor DEHP [di-(2-ethylhexyl) phthalate] exposure dose-dependently causes fetal IUGR (intrauterine growth restriction); mRNA levels of placental Thra1 (zeige THRA Proteine) and Thrb1 are reduced and nuclear translocation of placental Thra1 (zeige THRA Proteine) and Thrb1 is suppressed in DEHP-exposed mice.
Genetic Repression in Hypothyroidism Is Mediated by Thrb1.
Thyroid hormone receptor beta and NCOA4 (zeige NCOA4 Proteine) regulate terminal erythrocyte differentiation.
TRbeta protein, target gene expression, and metabolic adaptive changes can occur in individual tissues without necessarily being reflected by circulating TH and TSH concentrations
Using domain exchanges and individual amino acid switches between THRA1 (zeige THRA Proteine) and THRB2, three amino acids were identified in helix 10 of the THRB2 ligand-binding domain that are required for negative regulation and are absent in THRA1 (zeige THRA Proteine).
Data suggest a novel role for THRbeta1 in secondary ossification at the epiphysis that involves transcriptional upregulation of Ihh (zeige IHH Proteine) gene.
In thyroid receptor-deficient mice, hair follicle stem cells present a clear defect in their mobilization (exit of their quiescent state and migration out of the niche), associated with increased activation of Smad (zeige SMAD1 Proteine) signaling.
Data show that TRbeta deficiency causes dysfunction of the monoaminergic system, accompanied by epigenetic disruption during the brain maturation process.
Results suggest mutually shared roles for thyroid hormone receptor beta isoforms TRbeta1 and TRbeta2 in cochlear development.
Our findings indicated that synergistic signaling of KRAS(G12D) and TRbetaPV led to increased MYC (zeige MYC Proteine) expression.
Data provide evidence that zebrafish represents a valid model to study in vivo the thyroid hormone (zeige PTH Proteine) (TH) action, and the molecular mechanisms underlying the two syndromes of TH resistance, RTHa and RTHb.
Data suggest that the embryonic to larval transitory phase is characterized by its dependency on the timely synthesis of thyroid hormone (zeige PTH Proteine) and the concomitant autoinductive increase in thyroid hormone receptor beta mRNA levels.
Report of a novel mutation T273R in the THRB gene of patients exhibiting signs of the syndrome of resistance to thyroid hormone (zeige PTH Proteine). Authors propose that the trans-activating function of TRbeta (zeige TXNRD2 Proteine) is likely dominantly hindered in these patients.
Authors previously shown that Nuclear Receptor Corepressor 1 (NCoR (zeige NCOR1 Proteine)) and the thyroid hormone receptor (zeige THRA Proteine) beta1 (TRbeta (zeige TXNRD2 Proteine)) inhibit tumor invasion. Here they show that these molecules repress VEGF-C (zeige VEGFC Proteine) and VEGF-D (zeige Figf Proteine) gene transcription in breast cancer cells, reducing lymphatic vessel density and sentinel lymph node invasion in tumor xenografts.
The results emphasized the importance of TRB1 (zeige TRIB1 Proteine) in the regulation of HSV-1 replication in differentiated environment with neuronal phenotype.
In certain contexts, Rb loss enables TRbeta1-dependent suppression of SKP2 as a safeguard against RB1 (zeige RB1 Proteine)-deficient tumorigenesis. TRbeta2 counteracts TRbeta1, thus disrupting this safeguard and promoting development of RB1 (zeige RB1 Proteine)-deficient malignancies.
A relatively stable genome in retinoblastoma tumor cells is maintained by TRb1 (zeige TRIB1 Proteine) and TRb2 (zeige TRIB2 Proteine)-mediated PTTG1 (zeige PTTG1 Proteine) inhibition, counteracting Rb-deficiency-related genomic instability.
the actions of R429Q-TRbeta1 in Resistance to Thyroid Hormone (RTH)-Syndrome most likely reflect the reduced hormone affinity observed for this mutant rather than an alteration in target gene repertoire.
The present studies uncovered a novel mechanism by which thyroid hormone receptor beta could function as a tumor suppressor through modulation of TNF alpha-IkappaB alpha-NFkappaB pathway.
Novel THRB single nucleotide substitution-C to G in codon 340 in resistance to thyroid hormone (zeige PTH Proteine) syndrome.
THRA (zeige THRA Proteine) predominates in multipotent human adipose derived stem cells (hADSC) whereas THRB is expressed at lower levels and is upregulated during hADSC differentiation.
Increased expression of mammary TRbeta1 and DIO2 (zeige DIO2 Proteine), and decreased RXRalpha (zeige RXRA Proteine), provide a mechanism to increase thyroid hormone (zeige PTH Proteine) activity within the mammary gland during lactation.
The protein encoded by this gene is a nuclear hormone receptor for triiodothyronine. It is one of the several receptors for thyroid hormone, and has been shown to mediate the biological activities of thyroid hormone. Knockout studies in mice suggest that the different receptors, while having certain extent of redundancy, may mediate different functions of thyroid hormone. Mutations in this gene are known to be a cause of generalized thyroid hormone resistance (GTHR), a syndrome characterized by goiter and high levels of circulating thyroid hormone (T3-T4), with normal or slightly elevated thyroid stimulating hormone (TSH). Several alternatively spliced transcript variants encoding the same protein have been observed for this gene.
thyroid hormone receptor beta
, nuclear receptor subfamily 1 group A member 2
, thyroid hormone receptor beta isoform
, thyroid hormone receptor beta 3
, thyroid hormone receptor beta2delta
, thyroid hormone receptor, beta (avian erythroblastic leukemia viral (v-erb-a) oncogene homolog 2)
, TR beta
, thyroid hormone receptor beta 1
, thyroid hormone receptor beta 2
, thyroid hormone receptor beta-1
, oncogene ERBA2
, thyroid hormone nuclear receptor beta variant 1
, thyroid hormone receptor, beta (erythroblastic leukemia viral (v-erb-a) oncogene homolog 2, avian)
, thyroid hormone receptor beta2
, beta-thyroid hormone receptor