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Critical role for NF-kappaB-induced JunB in VEGF regulation and tumor angiogenesis.
TLDR
It is demonstrated that the AP-1 subunit junB is a target gene of hypoxia-induced signaling via NF-kappaB and identified JunB as a critical independent regulator of VEGF transcription and provides a mechanistic explanation for the inherent vascular phenotypes seen in JunB-deficient embryos, ex vivo allantois explants and in vitro differentiated embryoid bodies. Expand
Endothelium‐specific Cre recombinase activity in flk‐1‐Cre transgenic mice
TLDR
This work characterized regulatory regions of the mouse flk‐1 gene sufficient for endothelial cell‐specific expression of the LacZ reporter gene in transgenic mice and generated transgenic mouse lines that will be valuable for the conditional inactivation of floxed target genes in endothelial cells of the embryonic vascular system. Expand
Critical role for NF‐κB‐induced JunB in VEGF regulation and tumor angiogenesis
TLDR
It is demonstrated that the AP‐1 subunit junB is a target gene of hypoxia‐induced signaling via NF‐κB and identified JunB as a critical independent regulator of VEGF transcription and provides a mechanistic explanation for the inherent vascular phenotypes seen in JunB‐deficient embryos, ex vivo allantois explants and in vitro differentiated embryoid bodies. Expand
Junb regulates arterial contraction capacity, cellular contractility, and motility via its target Myl9 in mice.
TLDR
Conditional ablation of the transcriptional regulator Junb results in impaired arterial contractility in vivo and in vitro and establishes a molecular link between the activator protein-1 transcription factor subunit Junb and actomyosin-based cellular motility as well as cellular and vascular contractility by governing Myl9 transcription. Expand
JunB is required for endothelial cell morphogenesis by regulating core-binding factor β
TLDR
It is demonstrated that cell-autonomous endothelial functions of the AP-1 subunit JunB are required for proper endothelial morphogenesis both in vivo in mouse embryos with endothelial-specific ablation of JunB and in in vitro angiogenesis models. Expand
Inhibition of hypoxia-inducible factor activity in endothelial cells disrupts embryonic cardiovascular development.
TLDR
Results show that HIFs in endothelial cells are essential for embryonic heart and blood vessel development and control angiogenesis and vascular remodeling. Expand
Serglycin proteoglycan is sorted into zymogen granules of rat pancreatic acinar cells.
TLDR
This study identified a high-molecular-weight molecule in aggregated content proteins of zymogen granules of pancreatic acinar cells and deleted the serine/glycine repeat region in the serglycin core protein. Expand
Phenolic excipients of insulin formulations induce cell death, pro-inflammatory signaling and MCP-1 release
TLDR
Insulin formulations are cytotoxic in vitro and the toxic effects of excipients might explain inflammation of infusion sites in vivo. Expand
Stromal expression of MMP-13 is required for melanoma invasion and metastasis.
TLDR
An important role of MMP-13 in tumor growth and an unexpected role in organ-specific metastasis of melanoma cells are suggested. Expand
HIF in vascular development and tumour angiogenesis.
TLDR
The expression of a dominant-negative HIF mutant in endothelial cells inhibited endothelial sprouting and disrupted cardiovascular development in mouse embryos, demonstrating that endothelial HIF function is essential for embryogenesis and indicating that HIF inhibition might not be an ideal anti-tumour strategy. Expand
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