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Before mRNAs are exported to the cytoplasm, it is crucial to check each mRNA for structural and functional integrity. Eukaryotic cells use several different mechanisms, collectively known as mRNA surveillance, to look for irregularities in mRNAs. Irregular or aberrant mRNA are rapidly degraded by various enzymes. If a defective mRNA escapes the surveillance, it would be translated into a protein which would either be non-functional or not function properly. One of the primary irregularities in...

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Related Experiment Video

Updated: Jul 10, 2026

Evaluation of Exon Inclusion Induced by Splice Switching Antisense Oligonucleotides in SMA Patient Fibroblasts

Evaluation of Exon Inclusion Induced by Splice Switching Antisense Oligonucleotides in SMA Patient Fibroblasts

Published on: May 11, 2018

A Smad transcriptional corepressor.

D Wotton¹, R S Lo, S Lee

¹Cell Biology Program, Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

|April 13, 1999

Summary

The study reveals that Smad2-Smad4 complexes in the nucleus can either activate or repress transcription. This switch depends on whether they recruit coactivators or TGIF and histone deacetylases (HDACs).

Area of Science:

Molecular Biology
Cell Signaling
Gene Regulation

Background:

Transforming growth factor beta (TGF-beta) signaling is crucial for cellular processes.
Smad proteins, particularly Smad2 and Smad4, are key mediators of TGF-beta.
Transcriptional regulation by Smad complexes involves interactions with coactivators and corepressors.

Purpose of the Study:

To investigate the mechanisms of Smad2-mediated transcriptional regulation.
To identify novel Smad2-interacting proteins.
To elucidate the role of TGIF in TGF-beta signaling.

Main Methods:

Co-immunoprecipitation assays to identify Smad2-binding proteins.
Reporter gene assays to measure transcriptional activity.
Chromatin immunoprecipitation to assess promoter binding.

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Main Results:

TGIF was identified as a novel Smad2-binding protein.
TGIF functions as a transcriptional repressor.
Smad complexes can recruit either coactivators (like p300/CBP) for activation or TGIF and histone deacetylases (HDACs) for repression.

Conclusions:

The formation of transcriptional activation or repression complexes by Smad2-Smad4 is context-dependent.
The balance between coactivators and corepressors (like TGIF/HDACs) dictates the transcriptional outcome.
This provides a novel mechanism for fine-tuning TGF-beta responses.