期刊
NATURE CELL BIOLOGY
卷 15, 期 3, 页码 309-316出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb2699
关键词
-
类别
资金
- National Institutes of Health [RO1-HL069929, R01-AI100288, R01-AI080455, R01-AI101406, P01-CA023766]
- Radiation Effects Research Foundation (RERF-NIAID)
- W. H. Goodwin and A. Goodwin
- The Lymphoma Foundation
- Alex's Lemonade Stand
- The Geoffrey Beene Cancer Research Center at Memorial Sloan-Kettering Cancer Center
- The Peter Solomon Fund
- Australian National Health and Medical Research Council Biomedical Training Fellowship
- Leukemia and Lymphoma Society
- Italian Foundation for Cancer Research
- Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
Coordinating the balance between haematopoietic stem cell (HSC) quiescence and self-renewal is crucial for maintaining haematopoiesis lifelong. Equally important for haematopoietic function is modulating HSC localization within the bone marrow niches, as maintenance of HSC function is tightly controlled by a complex network of intrinsic molecular mechanisms and extrinsic signalling interactions with their surrounding microenvironment(1). In this study we demonstrate that nuclear factor erythroid 2-related factor 2 (Nfe212, or Nrf2), well established as a global regulator of the oxidative stress response, plays a regulatory role in several aspects of HSC homeostasis. Nrf2 deficiency results in an expansion of the haematopoietic stem and progenitor cell compartment due to cell-intrinsic hyperproliferation, which was accomplished at the expense of HSC quiescence and self-renewal. We further show that Nrf2 modulates both migration and retention of HSCs in their niche. Moreover, we identify a previously unrecognized link between Nrf2 and CXCR4, contributing, at least partially, to the maintenance of HSC function.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据