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.

Transcription factor Sox9 has an important role in neocortex expansion, where its expression in basal progenitors increases proliferation, induces premature gliogenesis and promotes the expression of extracellular matrix components.

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.

During aging, the pancreatic endocrine islets undergo chronic inflammation, which is associated with a reduced capacity for self-renewal of the insulin-producing beta-cells in zebrafish.

Depletion of PHF19 in prostate cancer cells leads to an increase in MTF2 and PRC2 chromatin occupancy causing deregulation of key genes critical for proliferation and metastasis.

The SCF-family of ubiquitin ligases regulates the key cancer proliferation node by controlling the degradation of RB-like tumor suppressor RBL2/p130.

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

Cellular acidity, capacity for net acid extrusion, and expression of acid-base transporters in human breast carcinomas independently predict variation in proliferative activity, lymph node metastasis, and patient survival.