Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Synthesis and Regulation of Thyroid Hormones01:20

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...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
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...
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Transport discovery of emerging robust helical surface States in Z2 = 0 systems.

Physical review letters·2014
Same author

Architectural properties of the neuromuscular compartments in selected forearm skeletal muscles.

Journal of anatomy·2014
Same author

Aromatic triazole foldamers induced by C-H···X (X = F, Cl) intramolecular hydrogen bonding.

The Journal of organic chemistry·2014
Same author

Human heat shock protein-specific cytotoxic T lymphocytes display potent antitumour immunity in multiple myeloma.

British journal of haematology·2014
Same author

ATG-Fresenius S combined with cyclosporine a: an effective immunosuppressive therapy for children with aplastic anemia.

Journal of pediatric hematology/oncology·2014
Same author

Priming of Toll-like receptor 4 pathway in mesenchymal stem cells increases expression of B cell activating factor.

Biochemical and biophysical research communications·2014

Related Experiment Video

Updated: May 30, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Study on the relationship between TSHR gene and thyroid diseases.

Li Shao1, Hua Jiang, Jun Liang

  • 1Department of Geratology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.

Cell Biochemistry and Biophysics
|August 11, 2011
PubMed
Summary

Single nucleotide polymorphisms in the Thyroid Stimulating Hormone Receptor (TSHR) gene were investigated for their role in common thyroid diseases. The study found no significant association between these TSHR gene polymorphisms and the pathogenesis of Graves

Related Experiment Videos

Last Updated: May 30, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

Area of Science:

  • Genetics
  • Endocrinology
  • Molecular Biology

Background:

  • The Thyroid Stimulating Hormone Receptor (TSHR) is implicated in the development of various thyroid disorders, including Graves' disease (GD), multinodular thyroid goiter (MTG), and Hashimoto's thyroiditis (HT).
  • Understanding the genetic underpinnings of these conditions is crucial for advancing diagnostic and therapeutic strategies.

Purpose of the Study:

  • To investigate whether single nucleotide polymorphisms (SNPs) within the TSHR gene contribute to the pathogenesis of common thyroid diseases.
  • To analyze the association between specific TSHR gene polymorphisms and the incidence of GD, MTG, and HT.

Main Methods:

  • A case-control study was conducted, examining eight TSHR gene SNPs in introns and exons.
  • DNA samples from patients with familial and sporadic thyroid diseases (GD, MTG, HT) and healthy controls were analyzed using direct sequencing.
  • A total of 184 individuals (patients and controls) were included in the genetic analysis.

Main Results:

  • Eight polymorphisms in the TSHR gene were identified, including a novel variant in exon 8 (AGA(Arg) → CGA(Arg)).
  • No statistically significant differences were observed in the frequency of these TSHR gene polymorphisms between patients with thyroid diseases and healthy control individuals.
  • Specific polymorphisms analyzed included variants in introns 1, 4, 5, 6, and exons 7 and 8.

Conclusions:

  • The investigated single nucleotide polymorphisms of the TSHR gene do not appear to be major contributors to the pathogenesis of the studied thyroid diseases.
  • Further research may be warranted to explore other genetic factors or regulatory elements influencing thyroid disease development.