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Details for anatomical structure: thyroid gland

EndoNet ID: ENC00145

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thyroid gland, thyroid body, thyroidea, Glandula thyroidea

General information

Endocrine ductless gland, consisting of irregularly spheroidal follicles, lying in front and to the sides of the upper part of the trachea, and is of horseshoe shape, with two lateral lobes connected by a narrow central portion, the isthmus; it secretes thyroid hormone and calcitonin

Links to other resources

Cytomer cy0052174

Larger structures


    • chief_cell_of_parathyroid_gland
    • cell:plasma_cell
    • mast_cell
    • mesenchyme_cell
    • macrophage
    • fibroblast

    Secreted hormones

    • Hormone: T4

      Influenced by:

      • thyroid stimulating hormone receptor
        in thyroid_gland
    • Hormone: T3

      Influenced by:

      • thyroid stimulating hormone receptor
        in thyroid_gland
    • Hormone: IL-13

      • IL-13 is an important mediator of antiinflammatory immune responses and is expressed in the thyroid and orbit. [1]
    • Hormone: CCL28

    • Hormone: calcitonin

    • Hormone: QRFP

    • Hormone: follicular dendritic cell secreted peptide

    • Hormone: katacalcin

    • Hormone: CGRP2

    • Hormone: slit-3 isoform 1


    • Receptor: GHS-R1

    • Receptor: GL-R

    • Receptor: CaSR

      Induced phenotype:

      • regulation of serum calcium levels
        • G protein-coupled extracellular calcium-sensing receptor regulates serum calcium levels by parathyroid hormone and calcitonin. [2]
        • G protein-coupled extracellular calcium-sensing receptor plays central role in calcium homeostasis by recognizing and responding to small changes in extracellular calcium, modulates functions of CaSR-expressing cells as to normalize the level of extracellular calcium. [3]
      • stimulation of phospholipase activity
        • G protein-coupled extracellular calcium-sensing receptor stimulates phospholipase C, A2, and D. [4]
      • inhibition of adenylate cyclase activity by G-protein signaling pathway
        • G protein-coupled extracellular calcium-sensing receptor inhibits adenylate cyclase through pertussis toxin-sensitive and -insensitive mechanisms. [3]
      • activation of MAPK cascade
        • G protein-coupled extracellular calcium-sensing receptor activates several mitogen-activated protein kinase (MAPK) cascades. [5]
      • neonatal hyperparathyroidism
        • Extracellular calcium ions are recognized as principal physiological regulators of parathyroid hormone secretion acting to close a endocrine feedback loop, whereby parathyroid hormone elevates extracellular calcium and in turn elevated extracellular calium suppresses parathyroid hormone secretion. [6]
        • Targeted deletion of CaSR eliminates feedback control of parathyroid hormone secretion and results in severe form of neonatal hyperparathyroidism. [6]
    • Receptor: thyroid stimulating hormone receptor

      Induced phenotype:

      • Graves-Basedow disease
        • Graves disease is an autoimmune thyroid disease characterized by the presence of antibodies against the thyrotropin receptor (TSHR), which result in constitutive activation of the receptor and increased levels of thyroid hormone, and stimulate the thyroid to cause hyperthyroidism and/or goiter. [7]
      • Hashimoto thyroiditis


      • T4
      • T3
    • Receptor: galanin receptor 3

    • Receptor: THRB1

      Induced phenotype:

      • 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. [8]
        • 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. [9]
        • 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. [10]
        • TR-β mutation, which is associated with the clinical syndrome of CRTH, dissociates positive and negative gene regulation by TH in vivo. [11]
    • Receptor: frizzled 1

    • Receptor: frizzled 2

    • Receptor: GFR-alpha-4

    • Receptor: NMU-R2

    • Receptor: hepatocyte growth factor receptor

    • Receptor: IL-28R-alpha-v2

    • Receptor: IL-28R-alpha-v1

    • Receptor: Sphingosine 1-phosphate receptor 2

      Induced phenotype:

      • regulation of cellular calcium homeostasis
        • Calcium entry is one of the main regulators of intracellular signaling. Calcium entry pathway is blocked by sphingosine, and activation of sphingosine kinase 1 (SK1) and the production of sphingosine 1-phosphate (S1P), through an autocrine mechanism, facilitate calcium entry through activation of S1P receptor 2. This is a novel mechanism by which the sphingosine-S1P rheostat regulates cellular calcium homeostasis. [12]
    • Receptor: relaxin receptor 2

    • Receptor: thyroid hormone receptor

      Induced phenotype:

      • Toxic multinodular goitre
        • Toxic multinodular goitre is a form of hyperthyroidism caused be excessive production of thyroid hormones. [13]
      • Hyperthyroidism
        • Resistance to thyroid hormone is an uncommon disorder, characterized by elevated circulating thyroid hormones with nonsuppressed thyrotropin levels, reflecting resistance within the hypothalamic-pituitary-thyroid axis but variable refractoriness to hormone action in peripheral tissues. [14]
      • Hypothyroidism
        • Hypothyroidism can be a result of either an absent thyroid gland or a deficiency in stimulating hormones from the hypothalamus or pituitary. [15]