A Na,K-ATPase beta subunit can suppress basal cell carcinogenesis either via its osmoregulatory function to avoid hypotonic stress, or by promoting epithelial polarity and adhesiveness of basal keratinocytes from the overlying outer layer.

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.

Linking deep mutational scanning with engineered transcriptional reporters in human cell lines establishes a generalizable method for exploring pharmacogenomics, structure, and function across broad classes of drug receptors.

The patterning of the nephron is driven by a gradient in the activity of β-catenin and further defined by a network of BMP, PTEN and NOTCH signalling.

Loss of mature β cell identity in diabetes can be prevented and rescued by small molecule inhibitors of the TGFβ pathway.

A new dynamic mechanistic model explains how the destruction complex negatively regulates Wnt signaling in development and oncogenesis.

Intercellular communication is critical for organ function, and the role of innervation in mediating this communication is of relevance to many fields, including developmental biology, neuroendocrinology, and disease pathophysiology.

Elevating beta-catenin signaling converts endothelial cells in typically fenestrated central nervous system vasculature to a blood-brain barrier (BBB) phenotype and promotes a BBB gene expression program and chromatin landscape.

Most regenerated cells after β-cell damage in zebrafish are Insulin+ Somatostatin+ bihormonal cells that are functional and able to restore glucose control.

Cells from the human pancreatic duct can be grown in culture and triggered to become insulin-producing cells, which could potentially be transplanted into patients with diabetes.