Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

Lethal Alleles

Lethal Alleles

Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...

You might also read

Related Articles

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

Sort by

Same author

The Missense Mutant ClC-5 (E211A), associated with Proton/Chloride Uncoupling Exacerbates Renal Pathology Compared to the ClC-5 null Mutant.

Kidney360·2026

Same author

Defining the safety and efficacy of liver-directed AAV gene therapy using a human liver tissue-equivalent platform.

Molecular therapy. Advances·2026

Same author

[Histone deacetylase 11 promotes ox-LDL-induced mouse macrophage foam cell formation via inhibiting autophagy].

Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology·2026

Same author

Database of <i>CLCN5</i> Pathogenic Variants Causing Dent Disease.

Kidney international reports·2026

Same author

Residential greenness exposure and preterm birth and small for gestational age: potential association, interaction with fine particle matter and mediation role of systemic immune inflammation.

Ecotoxicology and environmental safety·2026

Same author

Mesenchymal stem cell extracellular vesicles ameliorate radiation-caused dry mouth via modulating immune balance and cell metabolism.

Stem cell research & therapy·2025

Search research articles

Related Experiment Video

Updated: May 1, 2026

Author Spotlight: Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator

Author Spotlight: Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator

Published on: May 19, 2023

Mex3c mutation reduces adiposity partially through increasing physical activity.

Changjie Han¹, Yan Jiao², Qingguo Zhao²

¹Institute for Regenerative MedicineWake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USADepartment of Human Anatomy and EmbryologyThe Second Military Medical University, Shanghai 200433, ChinaInstitute for Regenerative MedicineWake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USADepartment of Human Anatomy and EmbryologyThe Second Military Medical University, Shanghai 200433, China.

The Journal of Endocrinology

|April 18, 2014

Summary

This summary is machine-generated.

The Mex3c gene mutation in mice increases physical activity, protecting against obesity and metabolic disorders. Neuronal Mex3c expression is key to regulating adiposity and physical activity levels.

Keywords:

Mex3c adiposity high-fat diet mice physical activity

More Related Videos

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Segmentation and Measurement of Fat Volumes in Murine Obesity Models Using X-ray Computed Tomography

Segmentation and Measurement of Fat Volumes in Murine Obesity Models Using X-ray Computed Tomography

Published on: April 4, 2012

Related Experiment Videos

Last Updated: May 1, 2026

Author Spotlight: Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator

Author Spotlight: Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator

Published on: May 19, 2023

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Segmentation and Measurement of Fat Volumes in Murine Obesity Models Using X-ray Computed Tomography

Segmentation and Measurement of Fat Volumes in Murine Obesity Models Using X-ray Computed Tomography

Published on: April 4, 2012

Area of Science:

Molecular Biology
Physiology
Genetics

Background:

The physiological function of MEX3C, an RNA-binding protein, is largely unknown.
Previous studies indicated Mex3c mutations in mice lead to growth retardation and reduced adiposity.
The precise mechanisms by which Mex3c influences adiposity require further elucidation.

Purpose of the Study:

To investigate the role of Mex3c in regulating adiposity and metabolic homeostasis.
To determine the impact of Mex3c mutations on physical activity levels.
To explore the contribution of neuronal Mex3c expression to adiposity regulation.

Main Methods:

Utilizing homozygous Mex3c gene trap mice and ob/ob mice.
Assessing physical activity levels in genetically modified mouse models.
Evaluating metabolic parameters including body weight, adiposity, glucose tolerance, insulin sensitivity, and lipid profiles.
Employing Cre-lox system to manipulate neuronal Mex3c expression.

Main Results:

Homozygous Mex3c gene trap mice exhibited significantly increased physical activity.
Mex3c mutation provided complete protection against diet-induced obesity, hyperglycemia, insulin resistance, hyperlipidemia, and hepatic steatosis.
In leptin-deficient ob/ob mice, the Mex3c mutation enhanced physical activity and improved glucose and lipid profiles.
Partial restoration of neuronal Mex3c expression led to increased white adipose tissue deposition.

Conclusions:

Mex3c regulates adiposity, at least in part, by modulating physical activity.
Neuronal Mex3c expression plays a critical role in controlling physical activity and adiposity.
Targeting Mex3c may offer a novel therapeutic strategy for metabolic disorders.