Acidic extracellular pH induces vascular endothelial growth factor (VEGF) in human glioblastoma cells via ERK1/2 MAPK signaling pathway: mechanism of low pH-induced VEGF. (Q38293986)

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scientific article published on 11 December 2001

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English	Acidic extracellular pH induces vascular endothelial growth factor (VEGF) in human glioblastoma cells via ERK1/2 MAPK signaling pathway: mechanism of low pH-induced VEGF.	scientific article published on 11 December 2001

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scholarly article

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Europe PubMed Central

PubMed publication ID

1 September 2017

Acidic extracellular pH induces vascular endothelial growth factor (VEGF) in human glioblastoma cells via ERK1/2 MAPK signaling pathway: mechanism of low pH-induced VEGF. (English)

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Europe PubMed Central

PubMed publication ID

1 September 2017

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Rakesh K Jain

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1 September 2017

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Dai Fukumura

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Lei Xu

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publication date

11 December 2001

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1 September 2017

Journal of Biological Chemistry

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1 September 2017

277

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1 September 2017

13

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1 September 2017

11368-11374

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1 September 2017

Role of vascular endothelial growth factor in the regulation of angiogenesis

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Angiogenesis in cancer and other diseases

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Expression of vascular endothelial growth factor and its receptors in the anaplastic progression of astrocytoma, oligodendroglioma, and ependymoma.

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Time-dependent vascular regression and permeability changes in established human tumor xenografts induced by an anti-vascular endothelial growth factor/vascular permeability factor antibody

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Hypoxic induction of vascular endothelial growth factor (VEGF) in human epithelial cells is mediated by increases in mRNA stability

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Acidosis inhibits endothelial cell apoptosis and function and induces basic fibroblast growth factor and vascular endothelial growth factor expression.

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Mitogen-activated protein kinase, ERK1/2, is essential for the induction of vascular endothelial growth factor by ionizing radiation mediated by activator protein-1 in human glioblastoma cells.

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Nuclear translocation of p42/p44 mitogen-activated protein kinase is required for growth factor-induced gene expression and cell cycle entry

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Activated MEK stimulates expression of AP-1 components independently of phosphatidylinositol 3-kinase (PI3-kinase) but requires a PI3-kinase signal To stimulate DNA synthesis

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ERK activation upon hypoxia: involvement in HIF-1 activation

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Identifiers

10.1074/JBC.M108347200

1 reference

Europe PubMed Central

PubMed publication ID

1 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

1 September 2017

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