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The developmental transcription factor DUX4 interacts with STAT1 and broadly suppresses expression of IFNγ-stimulated genes.

Rodent herpesvirus Peru overcomes NK ‘missing-self’ killing using a non-classical MHC-I like protein resistant todownregulation by its own ubiquitin ligase that potently sabotages antigen presentation to T-cells.

Oligodendroglia express major histocompatibility complex (MHC) pathways in response to inflammation and MHC reporter mice allow for the investigation of MHC molecule expressing cells in vivo.

Human leukocyte antigen class I (HLA class I) polymorphisms dictate the degree of endo-lysosomal assembly, which can supplement endoplasmic reticulum assembly for constitutive HLA class I expression and increase the efficiency of cross-presentation.

Skeletal muscle from world-class octogenarian athletes, representing a population with very high physical function in advanced age, exhibits greater mass and strength that is associated with overrepresentation of proteins involved in mitochondrial biology and more oxidatively competent muscle fibers.

Pre-existing enhancers interpret T cell signaling strength in an analogue manner to direct quantitative changes in gene expression within the context of an overall digital response.

Forward genetic screening has provided insight into the molecular mechanisms and stress pathways that promote tumor cell recognition by natural killer cells.

An unbiased genome-wide human forward genetic screen identifies the vacuolar ATPase complex and assembly factors as regulators of HIF stability through their actions on intracellular iron metabolism.

Iron derived from autophagy-mediated ferritin degradation in response to pressure overload induces lipid peroxidation, necrotic cardiomyocyte death, and heart failure in mice.

A new online data analysis platform, Mendelian Randomization for Alzheimer’s Disease (MRAD), enables the identification of risk or protective factors for Alzheimer’s disease.