In vivo imaging reveals that gradually increased amount of glucose mediates the heterogeneous functional development of individual β-cells by activating its major downstream calcineurin/NFAT signaling pathway.

Mechanicals forces and local (Wnt) signaling can synergize to increase β-catenin signaling and produce unique growth phenotypes.

Imaging of single cells within a cell population shows the correlation between subcellular accumulation of β-catenin and the transcriptional activation of a target gene.

β- and γ-cytoplasmic actins have different translation rates in cells and exert different nucleotide coding sequence-dependent effects on cell migration.

The membrane proteins Reck and Gpr124 are integral components of a novel Wnt7a/Wnt7b-specific signaling complex, and there is a distinctive requirement for Wnt/β-catenin signaling in tip cells during angiogenesis in the central nervous system.

Genetically modified mouse model and comprehensive analysis reveal the molecular mechanisms regulating early T-cell development through intracellular TCRβ expression-mediated β-selection and independent cell survival signaling.

The functional network of β-cells in the pancreatic islet, which has been used to identify important subpopulations of β-cells implicated in diabetes progression, is indicative of intrinsic dynamics rather than structural communication, implying islet robustness.

Under insulinopenic conditions, the hormone adiponectin is essential for lipid uptake specifically in subcutaneous white adipose tissue, and is sufficient to ameliorate islet lipotoxicity.

Alk5/TGF-β signaling is required in the endothelium to orchestrate zebrafish cardiac outflow tract morphogenesis, regulating smooth muscle cell and extracellular matrix organization.

mTORC1 inhibition by perinatal ER stress induces beta-cell growth arrest with subsequent development of diabetes.