Browse our latest Cell Biology articles

Replication stress-indepedent synthetic lethality can be triggered in BRCA2-deficient cells by exploiting M phase defects.

The transcription factor Nr2f1a represses ventricular and pacemaker cardiomyocyte identities within distinct regions of the zebrafish atrium.

The Dictyostelium discoideum TRAF6 homolog TrafE coordinates the autophagy and ESCRT membrane repair machineries and works in the major cell-autonomous restriction pathway to control Mycobacterium marinum intracellular infection.

Single-cell transcriptomic analysis reveals novel regenerative endothelial cell populations that mediate remarkably rapid and complete microvascular repair in a novel model of acute lung injury induced by endothelial cell ablation.

Kazrin, a protein widely expressed in vertebrates whose depletion causes defects in cell adhesion and migration, is recruited to early endosomes and promotes dynein/dynactin-dependent traffic of endocytosed cargo to the recycling endosomes.

A refined analysis of the mechanisms controlling CaM kinase-1 subcellular localization in sensory neurons, a cell-autonomous process known to control nociceptive plasticity and to adjust avoidance behaviors.

Microtubule-dependent movement of the glucose transporter GLUT4 is important for insulin-stimulated muscle glucose uptake, involves the motor protein KIF5B, and is impaired in muscle from diet-induced obese mice.

Loss or PTH1R-mediated repression of Zfp467 results in a pathway that increases Pth1r transcription via NFκB1 and thus cellular responsiveness to PTH/PTHrP, ultimately leading to enhanced bone formation.

High-resolution live and fixed tissue imaging combined with cell and tissue scale data analyses revealed that a ratchet-like constriction of the apical surfaces of cells drives the first step of an epithelial-to-mesenchymal transition taking place during mouse gastrulation.

Nearly half of the transcriptome is altered when endothelial cells transition in vitro, expression patterns for some genes are regained by exposing cells to shear stress and others through exposure to smooth muscle cells.