Biofoundries are a nucleating hub for industrial translation.

Contemporary synthetic biology embraces the entire innovation pipeline; it is a transformative technology platform impacting new applications and improving existing industrial products and processes. However, challenges still emerge at the interface of upstream and downstream processes, integral to the value chain. It is now clear that biofoundries have a key role to play in addressing this; they provide unique and accessible infrastructure to drive the standardization necessary to deliver systematic design and engineering of biological systems and workflows.

Differences in the mechanism of metabolic regulation of ATP-sensitive K+ channels containing Kir6.1 and Kir6.2 subunits.

Aims: ATP sensitive K(+) channels (K(ATP)) sense adenine nucleotide concentrations and thus couple the metabolic state of the cell to membrane potential. The hetero-octameric complex of a sulphonylurea receptor (SUR2B) and an inwardly rectifying K(+) channel (Kir6.1) and the corresponding native channel in smooth muscle are relatively insensitive to variations in intracellular ATP.

Metacaspase-8 modulates programmed cell death induced by ultraviolet light and H2O2 in Arabidopsis.

Programmed cell death (PCD) is a genetically controlled cell death that is regulated during development and activated in response to environmental stresses or pathogen infection. The degree of conservation of PCD across kingdoms and phylum is not yet clear; however, whereas caspases are proteases that act as key components of animal apoptosis, plants have no orthologous caspase sequences in their genomes. The discovery of plant and fungi metacaspases as proteases most closely related to animal caspases led to the hypothesis that metacaspases are the functional homologues of animal caspases in these organisms.

Complex ABCC8 DNA variations in congenital hyperinsulinism: lessons from functional studies.

Objective: Congenital hyperinsulinism (CHI) is a cause of persistent and severe hypoglycaemia in infancy. Mutations in the genes ABCC8 and KCNJ11 encoding SUR1 and Kir6.2, respectively, are the commonest cause of CHI.