Putting the brakes on transcription at damaged chromatin: Do Polycomb silencers do more than modify histones?

Younghoon Kee

doi:10.1080/23723556.2016.1244513

Putting the brakes on transcription at damaged chromatin: Do Polycomb silencers do more than modify histones?

Younghoon Kee

Department of New Biology

Research output: Contribution to journal › Article › peer-review

Abstract

One of the cellular responses to DNA damage is to monitor and execute temporary arrest of RNA synthesis at chromatin lesions. The Polycomb silencer BMI1 is a well-known contributor to this process. We recently described a new mode of BMI1-mediated transcription arrest at lesions that involves UBR5 E3 ligase and FACT histone chaperon.

Original language	English
Article number	e1244513
Journal	Molecular and Cellular Oncology
Volume	3
Issue number	6
DOIs	https://doi.org/10.1080/23723556.2016.1244513
State	Published - 1 Nov 2016

Bibliographical note

Publisher Copyright:
© 2016, © 2016 Taylor & Francis Group, LLC.

Keywords

BMI1
FACT
Polycomb

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1080/23723556.2016.1244513

Cite this

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abstract = "One of the cellular responses to DNA damage is to monitor and execute temporary arrest of RNA synthesis at chromatin lesions. The Polycomb silencer BMI1 is a well-known contributor to this process. We recently described a new mode of BMI1-mediated transcription arrest at lesions that involves UBR5 E3 ligase and FACT histone chaperon.",

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AB - One of the cellular responses to DNA damage is to monitor and execute temporary arrest of RNA synthesis at chromatin lesions. The Polycomb silencer BMI1 is a well-known contributor to this process. We recently described a new mode of BMI1-mediated transcription arrest at lesions that involves UBR5 E3 ligase and FACT histone chaperon.

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KW - Polycomb

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Putting the brakes on transcription at damaged chromatin: Do Polycomb silencers do more than modify histones?

Abstract

Bibliographical note

Keywords

UN SDGs

Access to Document

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