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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Hypothyroidism II: Pathophysiology01:23

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...
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...

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Hypothyroidism and hyperthyroidism modulates Ras-MAPK intracellular pathway in rat thyroids.

Anna Lúcia R C Leal1, Thiago U Pantaleão, Débora G Moreira

  • 1Laboratório de Fisiologia Endócrina, Instituto de Biofísica Carlos Chagas Filho, UFRJ, CCS-bloco G, Rio de Janeiro, 21949-900, Brazil.

Endocrine
|September 18, 2007
PubMed
Summary

Thyrotropin (TSH) may stimulate rat thyroid cell proliferation via Ras signaling. However, extracellular signal-regulated kinase (ERK) phosphorylation does not appear to be involved in this TSH-induced pathway.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Signaling

Background:

  • Thyrotropin (TSH) regulates thyroid cell proliferation and function via a G protein-coupled receptor.
  • The precise intracellular signaling pathways mediating TSH-induced thyrocyte proliferation in vivo remain incompletely understood.

Purpose of the Study:

  • To investigate whether TSH induces Ras activation in rat thyroids.
  • To determine the involvement of extracellular signal-regulated kinase (ERK) in the TSH-induced intracellular signaling cascade.

Main Methods:

  • Hypothyroidism was induced in Wistar rats using methimazole (MMI).
  • Hyperthyroidism was induced by T4 administration.
  • Ras modulation and ERK phosphorylation (pERK) levels were analyzed in thyroid tissues.

Main Results:

  • Hypothyroid rats showed increased Ras modulation but decreased pERK.
  • Rats with T4-induced hyperthyroidism exhibited increased thyroidal pERK without significant changes in Ras.
  • These findings suggest a dissociation between Ras/ERK pathways in TSH-stimulated thyroid growth.

Conclusions:

  • TSH-induced rat thyroid proliferation may involve enhanced Ras signaling.
  • The downstream signaling cascade does not appear to involve ERK phosphorylation, which increases during T4-induced hyperthyroidism.