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The transition from a restrictive patterning mechanism to one sensitive to a variety of environmental cues in NOTCH-mediated angiogenesis offers crucial insights into vascularization in damaged organs and cancer therapy.

The interplay between the transcriptional co-regulators YAP1/TAZ and the hypoxia-controlled transcription factor HIF1α differentially regulates endothelial cell behavior in the hypoxic environment of bone compared to other organs.

Increasing levels of the growth factor Vegfa disrupt blood vessel branching morphogenesis and drive diameter increase by synchronizing Notch signalling fluctuations between endothelial cells.

Endothelial YAP/TAZ shape the developing vasculature by orchestrating mechanical inputs with BMP signalling to promote junctional VE-Cadherin turnover and cellular rearrangements.

Single cell transcriptomics reveal a complex orchestration of lung immune cells during the transition from fetal to air-breathing life to fill context-specific functions in tissue remodeling, angiogenesis, and immunity.

Primary cilia on endothelial cells are required for VEGF-A/ VEGFR2-dependent signaling, islet vascularization and, consequently, nutrient delivery and insulin disposal.

A novel molecular strategy to block transcription factor activity using small molecule interference of multiple protein-protein interactions is reported.

ZHX2 controls HIF1α oncogenic signaling and tumorigenesis in triple-negative breast cancer.

Analyses with genetically engineered mouse models in combination with biochemical approaches reveal a crucial role of the receptor tyrosine kinase Tie2 mediated signals in venogenesis via an Akt mediated regulation of COUP-TFII protein stabilization.

Identification of a developmental mechanism critical for the generation of brain vessel heterogeneity.