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Related Experiment Video

Updated: Jul 13, 2026

An Optimized Protocol for Electrophoretic Mobility Shift Assay Using Infrared Fluorescent Dye-labeled Oligonucleotides

An Optimized Protocol for Electrophoretic Mobility Shift Assay Using Infrared Fluorescent Dye-labeled Oligonucleotides

Published on: November 29, 2016

SOX18 directly interacts with MEF2C in endothelial cells.

B M Hosking¹, S C Wang, S L Chen

¹Institute for Molecular Bioscience, University of Queensland, Brisbane 4072, Queensland, Australia.

Biochemical and Biophysical Research Communications

|September 14, 2001

Summary

The transcription factors MEF2C and SOX18 directly interact and are coexpressed in endothelial cells. MEF2C enhances SOX18

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Isolation of Primary Murine Skeletal Muscle Microvascular Endothelial Cells

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Area of Science:

Molecular Biology
Developmental Biology
Genetics

Background:

Mutations in the Sry-related HMG box gene Sox18 cause vascular and hair follicle defects in mice.
SOX18 and MADS box transcription factor MEF2C are expressed in developing endothelial cells.
Null mutants of Sox18 and Mef2c exhibit overlapping phenotypic abnormalities.

Purpose of the Study:

Investigate the relationship between SOX18 and MEF2C DNA binding proteins.
Determine if MEF2C and SOX18 interact and their functional relationship in vivo.
Understand the role of MEF2C-SOX18 interaction in vascular development.

Main Methods:

Co-immunoprecipitation to assess protein interaction.
Immunofluorescence to confirm coexpression in endothelial cell nuclei.
In vivo transcriptional assays to evaluate functional synergy.

Main Results:

Direct physical interaction between MEF2C and SOX18 proteins was confirmed.
MEF2C and SOX18 are coexpressed in endothelial cell nuclei in vivo.
MEF2C potentiates SOX18-mediated transcription and regulates its activation domain.
MEF2C does not interact with or co-activate transcription with mutant SOX18 proteins (Ra, RaJ).

Conclusions:

MEF2C and SOX18 are important functional partners in transcriptional regulation.
Their interaction is crucial for normal vascular development.
Mutations in SOX18 disrupt the interaction with MEF2C, leading to developmental defects.