ECM-Itgb1 signaling and cell-cell adhesion are pivotal and coordinate together to regulate pancreatic islet aggregation, architecture, and functional maturation during development.

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.

Combinations of transcription factors can convert pancreatic acinar cells into endocrine α-, β- and δ-cells in vivo.

Human pancreatic islet high-resolution chromatin state maps generated from DNA methylation, open chromatin and ChIP-seq mark data facilitate the characterisation of regulatory mechanisms at type 2 diabetes genome-wide association study loci.

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.

Analysis of islet calcium oscillation responses will provide the field with a resource with which to determine the strain of interest for their specific islet biology questions.

Combination of deep learning models trained on tissue-specific genomic data and fine-mapping approaches supports efforts to identify causal variants and mechanisms at GWAS loci.

Synchronized β cell response to glucose is lost concomitant with loss of islet architecture in Robo-deficient islets of Langerhans in vivo.

Proton channels are present in reef-building corals and constitute important molecular players that should help understand calcification and the response of these organisms to ocean acidification.

A mouse model of maturity-onset diabetes of the young illuminates that overactive TALK-1 channels limit β-cell calcium influx through membrane potential hyperpolarization, which blunts insulin secretion and causes glucose intolerance.