Tracking of all cells in intestinal organoids crypts to fully reconstruct cell lineages reveals that proliferative behavior is highly symmetric between sisters cells, while simulations show that this observed symmetry minimizes random fluctuations in cell proliferation, thereby ensuring homeostasis.

Systematic CRISPR-based editing of tRNA genes revealed that different human cells that span a range of growth rates and different modes of proliferation states require diverse tRNA sets.

Single-cell RNA sequencing reveals Nrg1/ErbB2-induced metabolic reprogramming as a pivotal event for cardiomyocyte proliferation during heart regeneration.

Src, an oncogene, promotes both cell proliferation and cell death simultaneously, which can be regulated by dietary methionine.

Hypoxia does not increase glycolysis in proliferating primary cells and antagonizes the increase in glycolysis caused by activation of hypoxia-inducible factor in normoxia, in part, through activation of MYC signaling pathways.

Loss of full-length dystrophin expression causes significant molecular and functional defects in human and mouse myoblast, thus closing the vicious cycle of DMD pathology.

Combined genetic experiments and cellular trafficking assays in Drosophila and mammalian models uncover a new role of RAS-like GTPases in EGFR signalling activation during tissue regeneration and tumourigenesis through regulation of EGFR internalisation.

Antigen Ki-67, which is widely used as a cell proliferation marker, controls heterochromatin organisation and gene expression.

In addition to increasing glycolysis, some proliferating cells exhibiting the Warburg effect also increase oxidative phosphorylation through mitochondrial fusion.

A microRNA-mediated mechanism coordinates cell proliferation with cell rearrangements during tissue morphogenesis.