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.

Genetic mouse models identify a critical mechanism of myogenic vasoconstriction and reveal the in vivo function of myogenic autoregulation in protecting from organ overperfusion and in maintaining vascular resistance.

Rescue of DUX4-induced muscle pathology by the RET inhibitor Sunitinib reveals the therapeutic potential for treatment of Facioscapulohumeral muscular dystrophy using tyrosine kinase inhibitors.

The myopathic transcription factor DUX4 induces discordant dysregulation of transcript and protein levels, demonstrating a key role for post-transcriptional gene regulation in facioscapulohumeral muscular dystrophy.

Tissue-specific temporal regulators impinge on the VEGF/Delta-Notch pathway to vary tip cell selection pace yielding diverse densities of vascular network.

Flow-dependent remodeling of blood vessels is critical for normal physiology and for recovery from arterial blockage in disease; understanding its cellular mechanisms may lead to the development of treatments for patients that are deficient in this process following myocardial infarction or other vascular diseases.

Identification of a novel role for central nervous system-resident progenitors in the patterning of the vascular network around the developing spinal cord.

Building on previous work (St John et al., 2013), we explain why secondary infection by dengue virus is associated with more severe vascular disease than primary infection.

Nemo-like kinase is a key protein promoting the pathogenesis of spinal and bulbar muscular atrophy.

Genome-wide integration of transcriptome, accessible chromatin, and DNA methylome data from vascular endothelial cells lays the foundation for understanding the gene regulatory circuits that generate organ-specific vascular specialization.