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Details for receptor: THRB1

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EndoNet ID: ENR00659

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Synonyms

  • thyroid hormone receptor beta-1
  • thyroid receptor beta 1
  • THR1
  • TRbeta1
  • THRB1
  • TR3

General information

  • Expressed in lung. [1]
  • TRbeta1 and the variant TR-alpha2 mRNA were moderately expressed in approximately 75% of osteoblasts. [2]
  • Thyroid hormone receptors function by binding to specific thyroid hormone-responsive sequences in promoters of target genes and by regulating transcription. [3]
  • TR-beta1 levels are similar in the three cases (2.33 +/- 0.12 for HepG2, 2.08 +/- 0.36 for human primary hepatocytes, and 2.91 +/- 0.05 for human liver). [4]
  • Unliganded receptors are potent repressors, and ligand binding converts them to transcriptional activators. [3]
  • T3 receptors are expressed in a developmentally specific pattern, especially in the brain [5]

Links to other resources

UniProt P10828
Ensembl ENST00000456926

Subunit information

Sequence 
MTPNSMTEN GLTAWDKPK HCPDREHDW 
KLVGMSEAC LHRKSHSER RSTLKNEQS 
SPHLIQTTW TSSIFHLDH DDVNDQSVS 
SAQTFQTEE KKCKGYIPS YLDKDELCV 
VCGDKATGY HYRCITCEG CKGFFRRTI 
QKNLHPSYS CKYEGKCVI DKVTRNQCQ 
ECRFKKCIY VGMATDLVL DDSKRLAKR 
KLIEENREK RRREELQKS IGHKPEPTD 
EEWELIKTV TEAHVATNA QGSHWKQKR 
KFLPEDIGQ APIVNAPEG GKVDLEAFS 
HFTKIITPA ITRVVDFAK KLPMFCELP 
CEDQIILLK GCCMEIMSL RAAVRYDPE 
SETLTLNGE MAVTRGQLK NGGLGVVSD 
AIFDLGMSL SSFNLDDTE VALLQAVLL 
MSSDRPGLA CVERIEKYQ DSFLLAFEH 
YINYRKHHV THFWPKLLM KVTDLRMIG 
ACHASRFLH MKVECPTEL FPPLFLEVF 
ED
UniProt P10828

Binding hormones

  • T3

Anatomical structures with this receptor

  • paraventricular_nucleus_of_hypothalamus

    Influences

    • negative TRH

  • thyroid_gland

    Induced phenotypes

    • generalized autosomal-recessive thyroid hormone resistance
      • Acting in a dominant negative fashion, THR-β mutants cause RTH by interfering with the function of normal THRs. [7]
      • The syndrome of resistance to thyroid hormone (RTH), caused by mutations within the C terminus of TH receptor-β, is characterized by resistance to TH negative feedback at the pituitary and hypothalamus, with resulting TSH and TH elevation. [8]
      • Although most RTH mutations cause generalized resistance to TH (GRTH), such that affected individuals are euthyroid or hypothyroid despite high circulating TH levels, some RTH mutations may be clinically associated with isolated central resistance to TH (CRTH), such that peripheral sensitivity to TH action is preserved. [9]
      • TR-β mutation, which is associated with the clinical syndrome of CRTH, dissociates positive and negative gene regulation by TH in vivo. [10]

  • lung

  • retina

    • THRB expression pattern is more restricted, and is developmentally regulated. Its main expression sites are the liver, pituitary, inner ear, retina and several brain areas. [11]

  • pituitary_gland_of_diencephalon

    • THRB expression pattern is more restricted, and is developmentally regulated. Its main expression sites are the liver, pituitary, inner ear, retina and several brain areas. [11]

  • chondrocyte

  • osteoblast

  • liver

    • THRB expression pattern is more restricted, and is developmentally regulated. Its main expression sites are the liver, pituitary, inner ear, retina and several brain areas. [11]

  • hepatocyte

    Influences

    • positive APOA5
      • T3-activated TRbeta1 enhanced the activity of APOA5 DR4-driven promoter constructs. [4]
      • Treatment with T3 significantly increased APOA5 mRNA levels at 6 h, and a 2-fold induction was achieved after 24 h of T3 addition. [4]

  • macrophage

  • brain

    • THRB expression pattern is more restricted, and is developmentally regulated. Its main expression sites are the liver, pituitary, inner ear, retina and several brain areas. [11]

  • internal_ear

    • THRB expression pattern is more restricted, and is developmentally regulated. Its main expression sites are the liver, pituitary, inner ear, retina and several brain areas. [11]
Reference