Analyses of genetically engineered mouse models reveal the androgen receptor-independent properties of a luminal stem/progenitor cell in the prostate epithelium, and its ability to serve as a cell of origin for castration-resistant prostate cancer.
More than 30 published articles have suggested that a protein kinase called MELK is an attractive therapeutic target in human cancer, but three recent reports describe compelling evidence that it is not.
Hybrid brain network models predict neurophysiological processes that link structural and functional empirical data across scales and modalities in order to better understand neural information processing and its relation to brain function.
Sponges and ctenophores lack hypoxia-inducible factors, suggesting that the metazoan last common ancestor could have lived aerobically under severe hypoxia and did not need to regulate its transcription in response to oxygen availability.
Lower mitochondrial coenzyme Q was a consistent feature across multiple in vitro and in vivo models of insulin resistance and was sufficient to cause insulin resistance through increased mitochondrial oxidants.
Proteomics and functional genomics coupled to an antibody discovery pipeline revealed the influence of oncogenic RAS signaling on the cell-surface proteome and resulted in the discovery of potential therapeutic targets for RAS-driven cancers.
Antitumor (natural killer) NK cell responses are negatively regulated by interactions between NK cells and endogenous NKG2D ligands constitutively expressed on lymph node endothelial cells and super-induced on tumor-associated endothelium.