DNA damage-induced HSPC failure depends on ROS accumulation downstream of IFN-1 signaling and Bid mobilization

ABSTRACT: Targeted mouse mutants with inactivated Mixed-Lineage-Leukemia-5 (Mll5, MGI:1924825) alleles exhibit numerical, cell cycle and functional abnormalities in their hematopoietic stem and progenitor cell (HSPC) compartments, including hyper-proliferation of otherwise quiescent hematopoietic stem cells, lack of long-term reconstitution potential and profound radiation sensitivity. Most of the HSPC defects are secondary to increased levels of DNA damage and intracellular accumulation of reactive oxygen species (ROS). To obtain first insights into underlying molecular mechanisms, we performed Affymetrix gene chip analysis using total RNA isolated from FACS-sorted Lin-Sca1+Kit+ (LSK) cells of Mll5+/+ and Mll5-/- mice, both with and without prior long-term treatment with the ROS quencher N-Acetyl-L

ORGANISM(S): Mus musculus

SUBMITTER: Medhanie Mulaw 

PROVIDER: E-GEOD-85076 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress