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Updated: Jun 23, 2026
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Analysis of the c-KIT Ligand Promoter Using Chromatin Immunoprecipitation
Published on: June 27, 2017
p65/RelA binds and activates the beclin 1 promoter
Tamara Copetti1, Francesca Demarchi, Claudio Schneider
1LNCIB Laboratorio Nazionale Consorzio Interuniversitario Biotecnologie AREA Science Park, Trieste, Italy.
Autophagy
|May 22, 2009
Summary
The transcription factor p65/RelA directly regulates beclin 1 gene expression, controlling autophagy. This finding suggests p65/RelA plays a key role in T-cell function and immune system balance.
Area of Science:
- Molecular Biology
- Cellular Biology
- Immunology
Background:
- Autophagy is a fundamental cellular process crucial for maintaining homeostasis.
- The beclin 1 gene is a key regulator of canonical autophagy.
- The role of transcription factors in modulating autophagy requires further elucidation.
Purpose of the Study:
- To identify novel regulatory elements controlling beclin 1 gene expression.
- To investigate the role of p65/RelA in the regulation of autophagy.
- To explore the functional implications of p65/RelA-mediated autophagy in T-cell activation.
Main Methods:
- Identification of p65/RelA consensus binding sites in the beclin 1 promoter.
- Assessment of p65/RelA binding to the beclin 1 promoter using chromatin immunoprecipitation assays.
- Quantification of autophagy levels in human cell lines under basal and induced conditions.
- Analysis of autophagy in Jurkat cells following T-cell receptor activation.
Main Results:
- Novel p65/RelA consensus sites were identified in the beclin 1 promoter.
- p65/RelA was demonstrated to positively modulate canonical autophagy in multiple human cell lines.
- T-cell receptor activation in Jurkat cells led to increased p65/RelA binding to the beclin 1 promoter and enhanced autophagy.
Conclusions:
- p65/RelA is a novel positive regulator of beclin 1-dependent autophagy.
- The p65/RelA-beclin 1 axis represents a potential mechanism for regulating autophagy during T-cell activation.
- These findings suggest a role for p65/RelA in controlling T-cell homeostasis through autophagy modulation.
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