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Zebrafish (Danio rerio) Polyclonal THRB Primary Antibody for ELISA, WB - ABIN408742
Liu, Chan: Thyroid hormones are important for embryonic to larval transitory phase in zebrafish. in Differentiation; research in biological diversity 2002
Human Polyclonal THRB Primary Antibody for IHC, ELISA - ABIN1579929
Wang, Wei, Guan, Xue: Triiodothyronine regulates distribution of thyroid hormone receptors by activating AMP-activated protein kinase in 3T3-L1 adipocytes and induces uncoupling protein-1 expression. in Molecular and cellular biochemistry 2014
Using domain exchanges and individual amino acid switches between THRA1 (show THRA Antibodies) 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 (show THRA Antibodies).
Data suggest a novel role for THRbeta1 in secondary ossification at the epiphysis that involves transcriptional upregulation of Ihh (show IHH Antibodies) 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 (show SMAD1 Antibodies) 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 (show MYC Antibodies) expression.
T3 induces FGF21 (show FGF21 Antibodies) in cultured hepatocytes and this effect involves direct actions of TRbeta1, which binds a TRE (show TREH Antibodies) within intron 2 of FGF21 (show FGF21 Antibodies). But T3 induced most gene expression in liver independently of FGF21 (show FGF21 Antibodies).
TRbeta acts as a cytoplasmic, phosphotyrosine-dependent scaffold for the p85 (show ECM1 Antibodies) regulatory subunit of PI3K and the Src kinase (show CSK Antibodies) Lyn (show LYN Antibodies) in the absence of thyroid hormone (show PTH Antibodies).
TRbeta-related deafness originates outside of hair cells and that TRalpha (show GNAT1 Antibodies) and TRbeta play opposing, non-redundant roles in hair cells.
Luciferase expression driven by the midwavelength sensitive opsin intron 3-4 region was only slightly increased by THRB2, and rather enhanced by COUP-TFII (show NR2F2 Antibodies).
Data provide evidence that zebrafish represents a valid model to study in vivo the thyroid hormone (show PTH Antibodies) (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 (show PTH Antibodies) and the concomitant autoinductive increase in thyroid hormone receptor beta mRNA levels.
Authors previously shown that Nuclear Receptor Corepressor 1 (NCoR (show NCOR1 Antibodies)) and the thyroid hormone receptor (show THRA Antibodies) beta1 (TRbeta (show TXNRD2 Antibodies)) inhibit tumor invasion. Here they show that these molecules repress VEGF-C (show VEGFC Antibodies) and VEGF-D (show Figf Antibodies) 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 (show TRIB1 Antibodies) 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 (show RB1 Antibodies)-deficient tumorigenesis. TRbeta2 counteracts TRbeta1, thus disrupting this safeguard and promoting development of RB1 (show RB1 Antibodies)-deficient malignancies.
A relatively stable genome in retinoblastoma tumor cells is maintained by TRb1 (show TRIB1 Antibodies) and TRb2 (show TRIB2 Antibodies)-mediated PTTG1 (show PTTG1 Antibodies) 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 (show PTH Antibodies) syndrome.
THRA (show THRA Antibodies) predominates in multipotent human adipose derived stem cells (hADSC) whereas THRB is expressed at lower levels and is upregulated during hADSC differentiation.
TRbeta (show TXNRD2 Antibodies) suppressed Runx2 (show RUNX2 Antibodies) transcriptional activities, thus confirming TRbeta (show TXNRD2 Antibodies) regulation of Runx2 (show RUNX2 Antibodies) at functional thyroid hormone (show PTH Antibodies)-response elements. Significantly, these findings indicate that a ratio of the tumor-suppressor TRbeta (show TXNRD2 Antibodies) and tumor-promoting Runx2 (show RUNX2 Antibodies) may reflect tumor aggression and serve as biomarkers in biopsy tissues. The discovery of this TRbeta (show TXNRD2 Antibodies)-Runx2 (show RUNX2 Antibodies) signaling supports the emerging role of TRbeta (show TXNRD2 Antibodies) as a tumor supp...
results revealed that microRNA 200a inhibits erythroid differentiation by targeting PDCD4 (show PDCD4 Antibodies) and THRB
Increased expression of mammary TRbeta1 and DIO2 (show DIO2 Antibodies), and decreased RXRalpha (show RXRA Antibodies), provide a mechanism to increase thyroid hormone (show PTH Antibodies) 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