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.
Proinsulin misfolding, an established cause of diabetes in patients with INS gene mutations, is now observed in normal human pancreatic islets, and rodents with genetic predisposition to type 2 diabetes.
The activin receptor ALK7 regulates the adaptation of brown adipose tissue to nutrient availability by preventing over-activation of signaling pathways induced by fasting, allowing appropriate response to cold exposure.
Dissecting structural, cellular and molecular differences between transplanted and spontaneous mouse tumor models, highlighting their relevance for predicting the efficacy of anti-cancer treatments in patients.
Live-cell microscopy and genome-wide screens reveal how slow transitions in metabolism can underlie metabolic memory, providing a model for organisms demonstrating similar history-dependent behaviour and routes to improve industrial microbes.
Loss of an amino acid transporter and tissue depletion of nitric oxide worsens the intestinal function of CF mice, a finding that potentially explains variation in disease severity amongst CF individuals.
Synthetic single domain antibody libraries and a binder selection cascade encompassing ribosome and phage display enable the selection of conformation-specific binders against previously intractable membrane proteins within three weeks.
Mutations causing proinsulin misfolding trigger unfolded protein response and lead to impaired proliferation and reduced mTORC1 signalling of developing beta-cells in a patient-derived induced pluripotent stem cell disease model.