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Genetics, in vivo imaging, and unbiased chemical biology screens reveal that Trpv6 functions as a cellular quiescence regulator and delineates a Trpv6-mediated Ca²⁺ signaling pathway maintaining the quiescent state.

Flow cytometric isolation and fate mapping shows that neurosphere-initiating cells are highly mitotically active and persist only transiently in vivo, and are distinct from quiescent, long-lived neural stem cells.

The H3K4 methyltransferase Setd1b is intrinsically required for hematopoietic stem and progenitor cell homeostasis and regulates lineage specification in mice.

The ability of cartilaginous fishes to generate new cartilage through adulthood, and to spontaneously repair damaged cartilage, could shed light on novel cell-based therapies for cartilage injury in mammals.

Single-cell and bulk expression analyses reveal that HCMV latent infection drives cells towards a weaker immune-responsive state, which is important for its expression and reactivation.

Primate-specific miR-934 mediates neurogenesis and downstream neuronal differentiation processes, modulating the expression of genes associated with the subplate, a region most prominent in primates, emerging during early cortical development.

C. elegans germline stem cells become quiescent under starved conditions, and this quiescence maintains the stem cell state even in the absence of GLP-1/Notch signaling, which is otherwise essential for stem cell maintenance.

Using a lineage tracing model, it is demonstrated that adult murine hematopoiesis is contingent on the continuous output from HSCs, with quantitative contributions that are dependent on lineage-type and age.

Loss of a single organ, the planarian pharynx, triggers immediate proliferation and expansion of stem cells required to replace it.

Skeletal muscle organoids differentiated from human pluripotent stem cells offer a system for investigating myogenesis and satellite cell development with translational potential for muscular dystrophy modeling and therapy development.