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Updated: Jan 7, 2026

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
Published on: September 20, 2018
Signaling network model of chromatin
Stuart L Schreiber1, Bradley E Bernstein
1Department of Chemistry and Chemical Biology and Howard Hughes Medical Institute, Harvard University, 12 Oxford Street, Cambridge, MA 02138, USA. sls@slsiris.harvard.edu
Cellular signaling and chromatin share common principles. Modifications on receptor tyrosine kinases (RTKs) and histones create docking sites, ensuring robust, switch-like signaling crucial for epigenetic inheritance.
Area of Science:
- Molecular Biology
- Biochemistry
- Epigenetics
Background:
- Cellular signaling networks and chromatin structure are fundamental to biological processes.
- Receptor tyrosine kinases (RTKs) and histone proteins are key components involved in signal transduction and gene regulation, respectively.
Purpose of the Study:
- To explore common underlying principles between cellular signaling networks and chromatin.
- To exemplify similarities by focusing on signaling complexes at membrane receptors and nucleosomes.
Main Methods:
- Comparative analysis of signaling complexes at membrane receptors and nucleosomes.
- Examination of signal-transducing modifications on receptor tyrosine kinases (RTKs) and histone proteins.
- Assessment of how modifications create docking sites for enzyme-substrate interactions.
Main Results:
- Multiple signal-transducing modifications on RTKs and histones act as docking sites.
- These modifications facilitate the proximal association of enzymes and their substrates.
- Histone modifications, analogous to RTK modifications, promote switch-like signaling and signal robustness.
Conclusions:
- Common principles govern both cellular signaling and chromatin organization.
- Histone modifications may function similarly to RTK modifications, contributing to signal robustness and switch-like behavior.
- This perspective offers new insights into chromatin function and epigenetic inheritance.
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