May 20, 2015

Transcriptional profiling of Foxo3a and Fancd2 regulated genes in mouse hematopoietic stem cells

Genomics Data
Xiaoli LiQishen Pang


Functional maintenance of hematopoietic stem cells (HSCs) is constantly challenged by stresses like DNA damage and oxidative stress. Foxo factors, particularly Foxo3a, function to regulate the self-renewal of HSCs and contribute to the maintenance of the HSC pool during aging by providing resistance to oxidative stress. Fancd2-deficient mice had multiple hematopoietic defects, including HSC loss in early development and in response to cellular stresses including oxidative stress. The cellular mechanisms underlying HSC loss in Fancd2-deficient mice include abnormal cell cycle status, loss of quiescence, and compromised hematopoietic repopulating capacity of HSCs. To address on a genome wide level the genes and pathways that are impacted by deletion of the Fancd2 and Foxo3a, we performed microarray analysis on phenotypic HSCs (Lin(-)ckit(+)Sca-1(+)CD150(+)CD48(-)) from Fancd2 single knockout, Foxo3a single knockout and Fancd2-/-Foxo3a-/- double-knockout (dKO) mice. Here we provide detailed methods and analysis on these microarray data which has been deposited in Gene Expression Omnibus (GEO): GSE64215.

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Mentioned in this Paper

Fanconi Anemia
Biochemical Pathway
Microarray Analysis
DNA Repair
Nucleic Acid Hybridization Procedure
Transcription, Genetic

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