scholarly journals Spleen tyrosine kinase mediates angiotensin II‐ and vascular endothelial growth factor‐induced angiogenesis

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Cuneyt Kemal Buharalioglu ◽  
Fariborz A Yaghini ◽  
Chi Young Song ◽  
Hafiz U Ghafoor ◽  
Anne M Estes ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Vascular Endothelial ◽  
Spleen Tyrosine Kinase ◽  
Endothelial Growth Factor

Bleeding with vascular endothelial growth factor tyrosine kinase inhibitor: A network meta-analysis

2021 ◽  
Vol 157 ◽  
pp. 103186
Author(s):  
Avash Das ◽  
Somnath Mahapatra ◽  
Dhrubajyoti Bandyopadhyay ◽  
Santanu Samanta ◽  
Sandipan Chakraborty ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Meta Analysis ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

The fms-like tyrosine kinase, a receptor for vascular endothelial growth factor

Science ◽  
1992 ◽  
Vol 255 (5047) ◽  
pp. 989-991 ◽  
Author(s):  
C de Vries ◽  
J. Escobedo ◽  
H Ueno ◽  
K Houck ◽  
N Ferrara ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Kinase A

Increased production of vascular endothelial growth factor (VEGF) by angiotensin II in neuro-2A cells

1999 ◽  
Vol 25 (2) ◽  
pp. 79-88 ◽  
Author(s):  
Krishna Pada Sarker ◽  
Masanori Nakata ◽  
Toshihiro Nakajima ◽  
Isao Kitajima ◽  
Ikuro Maruyama
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Tat–Human Immunodeficiency Virus-1 Induces Human Monocyte Chemotaxis by Activation of Vascular Endothelial Growth Factor Receptor-1

Blood ◽  
1997 ◽  
Vol 90 (4) ◽  
pp. 1365-1372 ◽  
Author(s):  
Stefania Mitola ◽  
Silvano Sozzani ◽  
Walter Luini ◽  
Luca Primo ◽  
Alessandro Borsatti ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Human Immunodeficiency Virus ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Vascular Endothelial ◽  
Immunodeficiency Virus ◽  
Monocyte Chemotaxis ◽  
Endothelial Growth Factor ◽  
Hiv 1 ◽  
Human Immunodeficiency Virus 1

Human immunodeficiency virus-1 (HIV-1) Tat protein can be released by infected cells and activates mesenchymal cells. Among these, monocytes respond to Tat by migrating into tissues and releasing inflammatory mediators. In the present study, we have examined the molecular mechanism of monocyte activation by Tat, showing that this viral protein signals inside the cells through the tyrosine kinase receptor for vascular endothelial growth factor encoded by fms-like tyrosine kinase gene (VEGFR-1/Flt-1). Subnanomolar concentrations of Tat induced monocyte chemotaxis, which was inhibited by cell preincubation with vascular-endothelial growth factor-A (VEGF-A). This desensitisation was specific for VEGF-A, because it not was observed with FMLP. In addition, the soluble form of VEGFR-1 specifically inhibited polarization and migration induced by Tat and VEGF-A, thus confirming the common use of this receptor. Binding studies performed at equilibrium by using radiolabeled Tat showed that monocytes expressed a unique class of binding site, with a kd of approximately 0.2 nmol/L. The binding of radiolabeled Tat to monocyte surface and the cross-linking to a protein of 150 kD was inhibited specifically by an excess of cold Tat or VEGF-A. Western blot analysis with an antibody anti–VEGFR-1/Flt-1 performed on monocyte phosphoproteins immunoprecipitated by an monoclonal antibody antiphosphotyrosine showed that Tat induced a rapid phosphorylation in tyrosine residue of the 150-kD VEGFR-1/Flt-1. Taken together, these results suggest that biologic activities of HIV-1 Tat in human monocytes may, at least in part, be elicited by activation of VEGFR-1/Flt-1.

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