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Related Concept Videos

Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

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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...
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Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

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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...
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Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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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...
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Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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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...
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Histone Modification02:32

Histone Modification

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...
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Histone Modification02:32

Histone Modification

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Related Experiment Video

Updated: Apr 20, 2026

Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model
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Thyroid hormone increases bulk histones expression by enhancing translational efficiency.

Alberto Zambrano1, Verónica García-Carpizo, Raquel Villamuera

  • 1Instituto de Investigaciones Biomédicas "Alberto Sols," Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, 28029 Madrid, Spain.

Molecular Endocrinology (Baltimore, Md.)
|November 26, 2014
PubMed
Summary
This summary is machine-generated.

Thyroid hormone (T3) increases canonical histone levels independently of DNA replication. This occurs via enhanced translation of histone mRNA, mediated by increased eukaryotic translation initiation factor 4γ2 (EIF4G2) levels.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Endocrinology

Background:

  • Canonical histone expression is typically linked to DNA synthesis during the S phase of the cell cycle.
  • Replication-dependent histone mRNAs utilize a stem-loop motif for regulation by stem-loop binding protein (SLBP), rather than a poly(A) tail.

Purpose of the Study:

  • To investigate the effect of thyroid hormone on canonical histone levels.
  • To elucidate the mechanism by which thyroid hormone influences histone biosynthesis.
  • To explore the role of thyroid hormone in posttranscriptional gene regulation.

Main Methods:

  • Incubation of mouse embryonic fibroblasts and other cell lines with thyroid hormone (T3).
  • Analysis of histone mRNA, SLBP levels, and protein expression.
  • Assessment of translational efficiency and polysome association of histone mRNA.
  • Investigation of eukaryotic translation initiation factor 4γ2 (EIF4G2) expression and its regulation.
  • Chromatin immunoprecipitation to assess thyroid hormone receptor binding to the Eif4g2 promoter.

Main Results:

  • Thyroid hormone (T3) significantly increased total histone levels in various cell types, independent of DNA replication.
  • T3 did not alter histone mRNA or SLBP levels, indicating a posttranscriptional regulatory mechanism.
  • T3 enhanced histone mRNA translation, evidenced by increased relocation to heavy polysomes.
  • T3 upregulated both mRNA and protein levels of EIF4G2, with the thyroid hormone receptor binding to the Eif4g2 gene promoter.
  • Depletion of EIF4G2 abolished the T3-induced increase in histone levels.

Conclusions:

  • Thyroid hormones play a crucial role in the posttranscriptional regulation of histone biosynthesis in a cell cycle-independent manner.
  • Thyroid hormone-mediated induction of EIF4G2 is essential for increasing histone levels.
  • This study highlights a novel mechanism for regulating eukaryotic translation initiation through thyroid hormone modulation of EIF4G2.