Corpus ID: 44686979

Critical role for NF-kappaB-induced JunB in VEGF regulation and tumor angiogenesis.

  title={Critical role for NF-kappaB-induced JunB in VEGF regulation and tumor angiogenesis.},
  author={D. Schmidt and B. Textor and Oliver T. Pein and A. Licht and S. Andrecht and Melanie Sator-Schmitt and N. Fusenig and P. Angel and M. Schorpp-Kistner},
  journal={The EMBO journal},
  volume={26 3},
Regulation of vascular endothelial growth factor (VEGF) expression is a complex process involving a plethora of transcriptional regulators. The AP-1 transcription factor is considered as facilitator of hypoxia-induced VEGF expression through interaction with hypoxia-inducible factor (HIF) which plays a major role in mediating the cellular hypoxia response. As yet, both the decisive AP-1 subunit leading to VEGF induction and the molecular mechanism by which this subunit is activated have not… Expand
Emerging Role of AP-1 Transcription Factor JunB in Angiogenesis and Vascular Development
JunB appears to be a new angiogenic factor that induces endothelial cell migration and sprouting particularly in neurovascular interaction during vascular development and plays a role in tissue-specific vascular maturation processes during neurov vascular interaction in mouse embryonic skin and retina vasculatures. Expand
Loss of stromal JUNB does not affect tumor growth and angiogenesis
It is shown that ablation of Junb in stromal cells including endothelial cells, vascular smooth muscle cells and fibroblasts does not affect tumor growth in two different syngeneic mouse models, the B16‐F1 melanoma and the Lewis lung carcinoma model. Expand
Activating transcription factor 2 increases transactivation and protein stability of hypoxia-inducible factor 1alpha in hepatocytes.
Results show that protein stabilization of ATF-2 under hypoxic conditions is required for the induction of the protein stability and transactivation activity of HIF-1alpha for efficient hypoxia-associated gene expression. Expand
Members of the CREB/ATF and AP1 family of transcription factors are involved in the regulation of SOX18 gene expression
Functional analysis revealed that CREB acts as a repressor, while JunB, c-Jun and ATF3 act as activators of SOX18 promoter activity, indicating that a transcriptional network that includes CREB, Jun B, c -Jun and ATF3 could be involved in angiogenesis-related transcriptional regulation of the SoX18 gene. Expand
Junb controls lymphatic vascular development in zebrafish via miR-182
It is demonstrated that the oncogenic miR-182 is a novel JUNB target and attenuates foxo1 expression indicating that strictly balanced Foxo1 levels are required for proper lymphatic vascular development in zebrafish. Expand
Mechanisms of adaptive angiogenesis to tissue hypoxia
  • G. Fong
  • Biology, Medicine
  • Angiogenesis
  • 2008
Five topics are discussed which indicate that while mechanisms of oxygen-regulated HIF-α stability provide exciting opportunities for the development of angiogenesis or anti-angiogenesis therapies, it is also highly important to consider various other mechanisms for the optimization of these procedures. Expand
An NF-κB–Dependent Role for JunB in the Induction of Proinflammatory Cytokines in LPS-Activated Bone Marrow–Derived Dendritic Cells
A novel role is identified for JunB—that is, induction of proinflammatory cytokines in LPS-activated primary DCs with NF-κB acting not only as an inducer of JunB, but also as its transcriptional partner. Expand
Jun and JunD-dependent functions in cell proliferation and stress response
Data show that Jun is of critical importance for cellular protection against oxidative stress in fetal livers and fibroblasts, and Jun-dependent cellular senescence can be restored by activation of the epidermal growth factor receptor pathway. Expand
Pancreatic β-cells activate a JunB/ATF3-dependent survival pathway during inflammation
The findings identify ATF3 as a novel downstream target of JunB in the survival mechanism of β-cells under inflammatory stress in mice derived from Ubi-JunB transgenic mice. Expand
JunB promotes cell invasion and angiogenesis in VHL-defective renal cell carcinoma
JunB promotes tumor invasiveness and enhances angiogenesis in VHL-defective ccRCCs, and quantitative PCR array analysis revealed that JunB regulated multiple genes relating to tumor invasion andAngiogenesis. Expand