Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [RNA-seq]

We collected significant amount of phenotypic and mechanistic data from a ATF4 knockout mouse model and demonstrated that HSC defects with an aging-like phenotype (expanded pool of phenotypical HSCs, decreased number of functional HSCs, impaired repopulating and self-renewal capacities of HSCs and myeloid bias) occurred in the ATF4 KO mice, suggesting that not only ATF4 indeed represents a pivotal factor for adult HSC function but also we had successfully constructed an ideal and attractive model to study aging and aging-related disease. Overall design: This dataset contains RNA-seq experiments of long-term HSCs isolated from ATF4WT or ATF4 CKO mice.