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.

The protein Tristetraprolin promotes the decay of MyoD mRNA to maintain satellite cell quiescence.

Genetic and protein analyses in vitro and in vivo identifies Id4 as a novel regulator of stem cell quiescence in the adult hippocampus.

A low-level pulse of the nuclear Prospero protein is necessary and sufficient to cause neural progenitor cells to enter a quiescent state.

The acquisition of vascular quiescence during transition to adulthood is driven by distinct transcriptional and epigenetic programs of pro- and anti-angiogenic genes, with the most prominent effect on the suppression of TGFß family signaling.

The stem cells of the postnatal muscle allow postnatal muscle growth and repair and withdraw from the cell cycle when the tyrosine phosphatase Ptpn11 (Shp2) is inhibited or mutated in mice.

General stress response factors Msn2 and Msn4 activate glycolytic genes and promote acetyl-CoA accumulation to stimulate growth and proliferation of yeast cells under a nutrient-limiting condition, suggesting the unexpected interrelationship between carbohydrate metabolism and stress response.

Lin37 is essential for cell-cycle gene repression by the DREAM complex in cellular quiescence and a combined loss of Lin37 and Rb prevents cell-cycle exit in response to growth-limiting signals.

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.

The quiescence-driven mutational landscape reveals replication-independent mutagenesis as a novel evolutionary force.