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Master Transcription Regulators

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...

Master Transcription Regulators

Master Transcription Regulators

General Transcription Factors

General Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...

Transcription Factors

Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...

Transcription Factors

Transcription Factors

Regulation of Expression Occurs at Multiple Steps

Regulation of Expression Occurs at Multiple Steps

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Related Experiment Video

Updated: Mar 28, 2026

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol

In Vitro Differentiation of Human CD4⁺FOXP3⁺ Induced Regulatory T Cells (iTregs) from Naïve CD4⁺ T Cells Using a TGF-β-containing Protocol

Published on: December 30, 2016

FOXP3 can modulate TAL1 transcriptional activity through interaction with LMO2.

V Fleskens¹, M Mokry², A M van der Leun¹

¹Department of Cell Biology, Centre of Molecular Medicine, University Medical Centre Utrecht, Utrecht, The Netherlands.

|December 22, 2015

Summary

Forkhead Box P3 (FOXP3) acts as a tumor suppressor in T-cell acute lymphoblastic leukemia (T-ALL). It inhibits oncogenic TAL1-complex activity, reducing T-ALL cell viability and altering cell cycle progression.

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Area of Science:

Oncology
Molecular Biology
Gene Regulation

Background:

T-cell acute lymphoblastic leukemia (T-ALL) is often driven by aberrant TAL1 and LMO2 expression, crucial for thymocyte transformation.
The transcription factor FOXP3 is found in various cancers, including T-ALL, suggesting a potential role.

Purpose of the Study:

To investigate the role of FOXP3 in T-ALL pathogenesis.
To elucidate the molecular mechanisms by which FOXP3 influences T-ALL cells.

Main Methods:

Analysis of FOXP3 expression correlation with TAL1-complex target genes in T-ALL patient samples and cell lines.
Assessment of cell cycle progression and viability in FOXP3-expressing T-ALL cells.
In vitro binding assays to study FOXP3 and LMO2/TAL1 interactions.

Main Results:

Increased FOXP3 levels inversely correlated with TAL1-complex target gene expression in T-ALL.
FOXP3 expression altered cell cycle regulation and decreased viability in T-ALL cells.
FOXP3 directly binds LMO2, disrupting the LMO2-TAL1 interaction.

Conclusions:

FOXP3 functions as a tumor suppressor in T-ALL.
FOXP3 modulates TAL1 transcriptional activity, offering a novel therapeutic target for T-ALL.