The Notch-PDGFRβ axis suppresses brown adipocyte progenitor differentiation in early post-natal mice.

De novo brown adipogenesis holds potential in combating the epidemics of obesity and diabetes. However, the identity of brown adipocyte progenitor cells (APCs) and their regulation have not been extensively explored. Here, through in vivo lineage tracing and mouse modeling, we observed that platelet-derived growth factor receptor beta (PDGFRβ)+ pericytes give rise to developmental brown adipocytes but not to those in adult homeostasis.

The Notch-Pdgfrβ axis suppresses brown adipocyte progenitor differentiation in early postnatal mice.

Unlabelled: De novo brown adipogenesis holds potential in combating the epidemics of obesity and diabetes. However, the identity of brown adipocyte progenitor cells (APCs) and their regulation have not been extensively studied. Here through lineage tracing, we observed that PDGFRβ+ pericytes give rise to developmental brown adipocytes, but not to those in adult homeostasis.

Targeting PGM3 as a Novel Therapeutic Strategy in Co-Mutant Lung Cancer.

In non-small-cell lung cancer (NSCLC), concurrent mutations in the oncogene and tumor suppressor (also known as LKB1) confer an aggressive malignant phenotype, an unfavourability towards immunotherapy, and overall poor prognoses in patients. In a previous study, we showed that murine co-mutant tumors and human co-mutant cancer cells have an enhanced dependence on glutamine-fructose-6-phosphate transaminase 2 (GFPT2), a rate-limiting enzyme in the hexosamine biosynthesis pathway (HBP), which could be targeted to reduce survival of co-mutants. Here, we found that co-mutant cells also exhibit an increased dependence on -acetylglucosamine-phosphate mutase 3 (PGM3), an enzyme downstream of GFPT2.