Marieke A.G. Essers

TL;DR: It is shown that in response to treatment of mice with interferon-α (IFNα), HSCs efficiently exit G0 and enter an active cell cycle, raising the possibility for new applications of type I interferons to target cancer stem cells.

TL;DR: A homeostasis mechanism for sustaining cellular reactive oxygen species that is controlled by signalling pathways that can convey both negative (PI‐3K/PKB) and positive (Ras/Ral) inputs is outlined.

TL;DR: An evolutionarily conserved interaction of β-catenin with FOXO transcription factors, which are regulated by insulin and oxidative stress signaling, is reported, demonstrating a role for β-Catenin in regulating FOXO function that is particularly important under conditions of oxidative stress.

TL;DR: Flow cytometric, transcriptomic and functional data at single-cell resolution are integrated to quantitatively map early differentiation of human HSCs towards lineage commitment and provide a basis for the understanding of haematopoietic malignancies.

TL;DR: This work shows in mice that DNA damage is a direct consequence of inducing HSCs to exit their homeostatic quiescent state in response to conditions that model physiological stress, such as infection or chronic blood loss, and provides a mechanistic explanation for the universal accumulation of DNA damage in H SCs during ageing and the accelerated failure of the haematopoietic system in Fanconi anaemia patients.