Ignet

Gene Information

Gene symbol: VEGFA

Gene name: vascular endothelial growth factor A

HGNC ID: 12680

Synonyms: VEGF-A, VPF

Related Genes

#	Gene Symbol	Number of hits
1	ACTC1	1 hits
2	AGT	1 hits
3	ANGPT2	1 hits
4	FGF1	1 hits
5	FLT1	1 hits
6	IL1RL1	1 hits
7	KDR	1 hits
8	NRP1	1 hits
9	PGF	1 hits
10	PLAT	1 hits
11	RPL10	1 hits
12	SPG7	1 hits
13	VWF	1 hits

Related Sentences

#	PMID	Sentence
1	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
2	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
3	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
4	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
5	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
6	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
7	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
8	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
9	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
10	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
11	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
12	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
13	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
14	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
15	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
16	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
17	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
18	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
19	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
20	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
21	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
22	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
23	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
24	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
25	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
26	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
27	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
28	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
29	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
30	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
31	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
32	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
33	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
34	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
35	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
36	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
37	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
38	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
39	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
40	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
41	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
42	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
43	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
44	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
45	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
46	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
47	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
48	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
49	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
50	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
51	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
52	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
53	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
54	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
55	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
56	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
57	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
58	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
59	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
60	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
61	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
62	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
63	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
64	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
65	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
66	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
67	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
68	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
69	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
70	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
71	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
72	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
73	9621286	The ability of VEGF to be chemotactic for monocytes and to increase the activity of collagenase and plasminogen activator may have implications for renal development and renal disease.
74	9621286	In humans, the cellular actions of VEGF depend on binding to two specific receptors: Flt-1 and KDR.
75	9621286	The aims of this study were: (1) to localize VEGF receptor proteins in human renal ontogenesis; (2) to quantify VEGF binding in human fetal and adult kidney; and (3) to dissect the binding into its two known components: the KDR and Flt-1 receptors.
76	9621286	The latter aim was achieved by competitive binding of VEGF and placenta growth factor-2, which only binds to Flt-1.
77	9621286	By double-label immunohistochemistry, VEGF receptor proteins were localized solely to endothelial cells of preglomerular vessels, glomeruli, and postglomerular vessels.
78	9621286	In developing glomeruli, VEGF receptor protein appeared as soon as endothelial cells were positive for von Willebrand factor.
79	9621286	Placenta growth factor-2 displaced VEGF binding in all renal structures by approximately 60%.
80	9621286	VEGF receptor proteins thus were found only in renal endothelial cells.
81	9621286	A coexpression of both VEGF binding sites could be shown, with Flt-1 demonstrating the most abundant VEGF receptor binding sites in the kidney.
82	9736244	VEGF receptors 1 and 2 (fit-1 and flk-1) are endothelial-specific receptor tyrosine kinases.
83	9773782	In all of the healthy subjects and all of the patients except those with PGN (disease control subjects), VPF/VEGF protein and mRNA were detected mainly in podocytes.
84	9773782	However, in some PGN patients, VPF/VEGF protein was demonstrated clearly in MC as well as in podocytes, as some of the VPF/VEGF was colocalized with alpha-smooth muscle actin, a marker of activated MC, and VPF/VEGF mRNA was expressed by MC and podocytes.
85	9773782	The time between biopsy and disease onset was significantly shorter in PGN patients with than in those without mesangial VPF/VEGF expression (P < 0.01).
86	9773782	In all of the healthy subjects and all of the patients except those with PGN (disease control subjects), VPF/VEGF protein and mRNA were detected mainly in podocytes.
87	9773782	However, in some PGN patients, VPF/VEGF protein was demonstrated clearly in MC as well as in podocytes, as some of the VPF/VEGF was colocalized with alpha-smooth muscle actin, a marker of activated MC, and VPF/VEGF mRNA was expressed by MC and podocytes.
88	9773782	The time between biopsy and disease onset was significantly shorter in PGN patients with than in those without mesangial VPF/VEGF expression (P < 0.01).
89	9773782	In all of the healthy subjects and all of the patients except those with PGN (disease control subjects), VPF/VEGF protein and mRNA were detected mainly in podocytes.
90	9773782	However, in some PGN patients, VPF/VEGF protein was demonstrated clearly in MC as well as in podocytes, as some of the VPF/VEGF was colocalized with alpha-smooth muscle actin, a marker of activated MC, and VPF/VEGF mRNA was expressed by MC and podocytes.
91	9773782	The time between biopsy and disease onset was significantly shorter in PGN patients with than in those without mesangial VPF/VEGF expression (P < 0.01).
92	9930379	A potential role for angiotensin II-induced vascular endothelial growth factor expression in the pathogenesis of diabetic nephropathy?
93	9930379	Ang II can stimulate the release of vascular endothelial growth factor (VEGF) from human vascular tissues.
94	9930379	This review considers the potential clinical significance of Ang II-induced VEGF expression, if any, in the pathogenesis of diabetic nephropathy and retinopathy.
95	9930379	A potential role for angiotensin II-induced vascular endothelial growth factor expression in the pathogenesis of diabetic nephropathy?
96	9930379	Ang II can stimulate the release of vascular endothelial growth factor (VEGF) from human vascular tissues.
97	9930379	This review considers the potential clinical significance of Ang II-induced VEGF expression, if any, in the pathogenesis of diabetic nephropathy and retinopathy.
98	9930379	A potential role for angiotensin II-induced vascular endothelial growth factor expression in the pathogenesis of diabetic nephropathy?
99	9930379	Ang II can stimulate the release of vascular endothelial growth factor (VEGF) from human vascular tissues.
100	9930379	This review considers the potential clinical significance of Ang II-induced VEGF expression, if any, in the pathogenesis of diabetic nephropathy and retinopathy.
101	10769233	In addition, pax2.1 expression in the lateral cells of the pronephric primordium is required to restrict the domains of Wilms' tumor suppressor (wt1) and vascular endothelial growth factor (VEGF) gene expression to medial podocyte progenitors.
102	10864579	Vascular endothelial growth factor (VEGF), a potent mitogen, is expressed in podocytes in the glomerulus, and VEGF receptors (flt-1, KDR, and neuropilin-1) are present on endothelial cells and other cell types.
103	10864579	In contrast, mesangial flt-1 and KDR receptor staining were both clearly seen in biopsy samples from proliferative renal diseases.
104	10864579	In conclusion, flt-1, KDR, and neuropilin-1 are present on cultured HMC, and VEGF(165) induces HMC proliferation.
105	10864579	In addition, the flt-1 and KDR receptors are expressed in the mesangium in mesangioproliferative disease.
106	10864579	Vascular endothelial growth factor (VEGF), a potent mitogen, is expressed in podocytes in the glomerulus, and VEGF receptors (flt-1, KDR, and neuropilin-1) are present on endothelial cells and other cell types.
107	10864579	In contrast, mesangial flt-1 and KDR receptor staining were both clearly seen in biopsy samples from proliferative renal diseases.
108	10864579	In conclusion, flt-1, KDR, and neuropilin-1 are present on cultured HMC, and VEGF(165) induces HMC proliferation.
109	10864579	In addition, the flt-1 and KDR receptors are expressed in the mesangium in mesangioproliferative disease.
110	11150374	Vascular endothelial cell growth factor (VEGF) has recently been recognized as a potent regulator of angiogenesis, vascular survival, and vascular permeability.
111	11261688	Angiopoietin-1 (Ang-1) is a secreted growth factor which binds to and activates the Tie-2 receptor tyrosine kinase.
112	11261688	Ang-2 binds the same receptor but fails to activate it: hence, it is a natural inhibitor of Ang-1.
113	11261688	Ang-2 destabilises capillary integrity, facilitating sprouting when ambient vascular endothelial growth factor (VEGF) levels are high, but causing vessel regression when VEGF levels are low.
114	11261688	Tie-1 is a Tie-2 homologue but its ligands are unknown.
115	11261688	During glomerular maturation, podocyte-derived Ang-1 and mesangial-cell-derived Ang-2 may affect growth of nascent capillaries.