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Related Concept Videos

Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
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Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
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Hyperthyroidism I: Introduction01:25

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Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
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Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...

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An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
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Published on: April 17, 2013

Thyrotropin-releasing hormone analogs.

A O Colson1, M C Gershengorn

  • 1Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 50 South Drive, Bldg 50/4134, Bethesda, MD 20892, USA.

Mini Reviews in Medicinal Chemistry
|February 14, 2006
PubMed
Summary

Researchers developed new thyrotropin-releasing hormone (TRH) analogs that selectively target the TRH-R2 receptor. This breakthrough advances understanding of TRH receptor interactions and offers potential for new therapeutic strategies.

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Area of Science:

  • Endocrinology
  • Neuroscience
  • Pharmacology

Background:

  • Thyrotropin-releasing hormone (TRH) is a key regulator of the anterior pituitary and nervous systems.
  • TRH mediates its effects via class A G-protein coupled receptors.
  • The recent identification of a second TRH receptor subtype (TRH-R2) necessitates the development of selective analogs.

Purpose of the Study:

  • To review advances in the development of TRH analogs.
  • To elucidate the mechanism of interaction between TRH analogs and TRH receptors.
  • To highlight the discovery of TRH analogs with selective binding at TRH-R2.

Main Methods:

  • Review of existing literature on TRH analog development.
  • Analysis of structure-activity relationships for TRH analogs.
  • Pharmacological characterization of TRH analog binding to receptor subtypes.

Main Results:

  • Significant progress has been made in designing TRH analogs with improved properties.
  • Understanding of TRH receptor binding and signaling pathways has advanced.
  • TRH analogs demonstrating selective binding to TRH-R2 have been identified.

Conclusions:

  • The development of TRH analogs targeting specific receptor subtypes is a promising area of research.
  • Selective TRH-R2 agonists/antagonists could offer novel therapeutic applications.
  • Further research into TRH receptor pharmacology is warranted.