SETD1A protects HSCs from activation-induced functional decline in vivo-Reference-Cited by-同舟云学术

SETD1A protects HSCs from activation-induced functional decline in vivo

Published:2018-03-22 Issue:12 Volume:131 Page:1311-1324
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Arndt Kathrin¹,Kranz Andrea²,Fohgrub Juliane¹,Jolly Adrien³,Bledau Anita S.²,Di Virgilio Michela⁴,Lesche Mathias⁵,Dahl Andreas⁵,Höfer Thomas³,Stewart A. Francis²,Waskow Claudia¹⁶⁷⁸

Affiliation:

1. Regeneration in Hematopoiesis, Institute for Immunology, and

2. Genomics, Biotechnology Center, Center for Molecular and Cellular Bioengineering, Technische Universität (TU) Dresden, Dresden, Germany;

3. Theoretical Systems Biology, German Cancer Research Center, Heidelberg, Germany;

4. Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany;

5. Deep Sequencing Group SFB655, Biotechnology Center, and

6. Department of Medicine III, Faculty of Medicine, TU Dresden, Dresden, Germany;

7. Regeneration in Hematopoiesis, Leibniz Institute on Aging, Fritz Lipmann Institute, Jena, Germany; and

8. Faculty of Biological Sciences, Friedrich Schiller University, Jena, Germany

Abstract

Key Points SETD1A regulates DNA damage signaling and repair in HSCs and hematopoietic precursors in the absence of reactive oxygen species accumulation. SETD1A is important for the survival of mice after inflammation-induced HSC activation in situ.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/131/12/1311/1405820/blood806844.pdf

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2. In Vivo and In Vitro Characterization of the RNA Binding Capacity of SETD1A (KMT2F);International Journal of Molecular Sciences;2023-11-07

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