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Opportunity at Armed Forces Radiobiology Research Institute (AFRRI)

Mechanisms of Radiation-Induced Mammalian Cell Premature Senescence


Armed Forces Radiobiology Research Institute

RO# Location
15.61.00.B7495 Bethesda, MD 208895603


Name E-mail Phone
Xiao, Mang 301.295.2597


A long-term goal of our group is to understand the role of signal transduction pathways in regulating mammalian cell survival, apoptosis, and senescence after ionizing radiation (IR). We have a special interest in understanding the effects of REDD1 (regulated in development and DNA damage responses 1), a novel cell stress response gene, on IR induced cell apoptosis and senescence. REDD1 is a transcriptional target of p53 and plays a bi-function as pro-survival and pro-apoptotic factor in different stress-induced cell damage. However, the effects of REDD1 on radiation-injured cells have not been investigated. We recently demonstrated that REDD1protects human bone marrow hematopoietic microenvironment component (hematopoietic niche) osteoblast cells from gamma-radiation induced premature senescence. In this project, we will study the role and molecular mechanisms of REDD1 in radiation-induced premature senescence of mammalian cells. The signal transduction cascade in response to IR involving REDD1 and stress response factors p53, p16, p19, NFkB, RPA, p21, and mTOR signaling will be investigated. The endpoint of this project is to better understand the mechanisms of IR induced premature senescence and the protective effects of REDD1 on mammalian cells after irradiation.



Xiao M, Whitnall, M: Current Molecular Pharmacology 2: 122, 2009

Li XH, et al: Haematologica 95: 1996, 2010


Gamma-radiation; Apoptosis; Senescence; REDD1; p53/p21; Signal transduction; mTOR;


Citizenship:  Open to U.S. citizens
Level:  Open to Postdoctoral and Senior applicants
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