| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| To our knowledge this is the first study to report on and off rates for the VEGF : sFlk 1 interaction . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| Stimulation of HUVEC with VEGF before co culture enhanced the inhibitory effect of HUVEC on BMSC differentiation . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| Loss of SPARC mediated VEGFR 1 suppression after injury reveals a novel antiangiogenic activity of VEGF A . ^^^ Excess VEGF A increased CNV before injury because VEGFR 1 activation was silenced by secreted protein , acidic and rich in cysteine ( SPARC ) . ^^^ The transient decline of SPARC after injury revealed a temporal window in which VEGF A signaling was routed principally through VEGFR 1 . ^^^ These observations indicate that therapeutic design of VEGF A inhibition should include consideration of the level and activity of SPARC . . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| In this study , we demonstrate that SPARC inhibits DNA synthesis by > 90 % in human microvascular endothelial cells ( HMEC ) stimulated by the endothelial cell mitogen vascular endothelial growth factor ( VEGF ) . ^^^ The inhibition was also observed with a peptide from the follistatin like domain 2 , whereas peptides from SPARC domains 1 and 3 had no effect on VEGF stimulated DNA synthesis . ^^^ The inhibition of HMEC proliferation was mediated in part by the binding of VEGF to SPARC . ^^^ The binding of 125I VEGF to HMEC was reduced by SPARC and SPARC peptides from domain 4 in a concentration dependent manner . ^^^ In a radioimmune precipitation assay , peptides from SPARC domains 2 and 4 each competed with native SPARC for its binding to VEGF . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| Finally , as compared with cells before passage in animals , thrombospondin 1 , SPARC , and VEGF gene expression was also deregulated in cell lines isolated from primary tumors induced by BPV 1 transformants . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| In this study , we investigated the effects of five exogenous growth factors known to be expressed by gliomas [ epidermal growth factor ( EGF ) , basic growth factor ( bFGF ) , transforming growth factor beta ( TGF beta 1 , 2 ) and vascular endothelial growth factor ( VEGF ) ] . on MMP 2 and MMP 9 expression in an ependymoma , two grade 3 astrocytomas , a grade 3 oligoastrocytoma and a benign meningioma . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| Alterations in SPARC and VEGF immunoreactivity in epithelial ovarian cancer . ^^^ Recent work has shown that SPARC modulates the mitogenic activity of VEGF in normal endothelium . ^^^ This study examines the immunoreactivity of SPARC and VEGF associated with neoplastic transformation of the ovary . ^^^ METHODS : Immunostaining for VEGF and SPARC protein was performed on 62 archival specimens . ^^^ CONCLUSIONS : Immunoreactivity of SPARC and VEGF is heightened in association with ovarian carcinoma , with a distinct distribution of SPARC in the stroma of neoplastic ovaries and VEGF within tumor cells . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| Induction of SPARC by VEGF in human vascular endothelial cells . ^^^ Although SPARC derived peptide showed an angiogenic effect , intact SPARC itself inhibited the mitogenic activity of vascular endothelial growth factor ( VEGF ) for ECs by the inhibiting phosphorylation of flt 1 ( VEGF receptor 1 ) and subsequent ERK activation . ^^^ To clarify the role of SPARC in tumor growth and progression , we determined the effect of VEGF on the expression of SPARC in human microvascular EC line , HMEC 1 , and human umbilical vein ECs . ^^^ VEGF increased the levels of SPARC protein and steady state levels of SPARC mRNA in serum starved HMEC 1 cells . ^^^ Inhibitors ( SB 202190 and SB 203580 ) of p 38 , a mitogen activated protein ( MAP ) kinase , attenuated VEGF stimulated SPARC production in ECs . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| A consequence of SPARC recognition by alphaVbeta 5 is enhanced VEGF production . ^^^ Thus , prostate cancer cells expressing VEGF / VEGFR 2 will activate alphaVbeta 3 and alphaVbeta 5 on their surface and use these integrins to migrate toward SPARC in bone . ^^^ Within the bone environment , SPARC engagement of these integrins will stimulate growth of the tumor and further production of VEGF to support neoangiogenesis , thereby favoring the development of the metastatic tumor . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| Compared with CCs of 1 week , PDLs and ABCs after 2 weeks revealed relatively high levels of all analyzed mRNAs , viz . , for EGF , HGF , VEGF , TGFbeta 1 , collagen 1 ( COL 1 ) , osteonectin ( ON ) , fibronectin ( FN 1 ) , and MMP 13 . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| Moreover , sponges from old SPARC null and WT mice contained similar levels of VEGF that were significantly lower than those from young ( 4 6 months ) mice . ^^^ In contrast to fibroblasts from young SPARC null mice , dermal fibroblasts from old SPARC null mice did not migrate farther , proliferate faster , or produce greater amounts of VEGF relative to their old WT counterparts . ^^^ However , when stimulated with TGF beta 1 , primary cells isolated from the sponge implants , and dermal fibroblasts from both old SPARC null and WT mice , showed marked increases in VEGF secretion . ^^^ These data indicate that aging results in a loss of enhanced angiogenesis in SPARC null mice , as a result of the detrimental impact of age on cellular functions , collagen deposition , and VEGF synthesis . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| We found that excess VEGF C did not enhance the rate of lymphatic endothelial cell ( LEC ) migration , the density of lymphatic vessels , or the rate of functionality even though lymphatic hyperplasia was present early on . ^^^ These results suggest that whereas excess VEGF C may enhance early LEC proliferation and cause lymphatic vessel hyperplasia , it does not augment the physiological rate of migration or functionality , and by itself can not sustain any lasting effects on lymphatic size , density , or organization in regenerating adult skin . . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| In vitro , SPARC has antiangiogenic properties , including the ability to inhibit the proliferation and migration of endothelial cells stimulated by bFGF and VEGF . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| RESULTS : A widespread carcinogenic field effect was detected for more than 50 % of the genes analyzed including Bax , BFT , CDX 2 , COX 2 , DAPK , DNMT 1 , GSTP 1 , RARalpha , RARgamma , RXRalpha , RXRbeta , SPARC , TSPAN , and VEGF . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| Peripheral blood mononuclear cells ( PBMCs ) containing EPCs isolated from six consenting young , healthy , adult volunteers were then plated both on ( 1 ) sheets of the nanocomposite with the bioactive peptide , ( 2 ) sheets of the nanocomposite without the bioactive peptide , ( 3 ) culture dishes as control and then cultured in presence of vascular endothelial growth factor ( VEGF ) . ^^^ |
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| Interacting proteins: P15692 and P09486 |
Pubmed |
SVM Score :0.0 |
| In fact , gene array analyses demonstrated that the proapoptotic cytokine tumour necrosis factor related apoptosis inducing ligand ( TRAIL ) inhibited mRNA expression of VEGF , along with those of matrix metalloproteinase 2 ( MMP 2 ) , its inhibitor tissue inhibitor of matrix metalloproteinases 2 ( TIMP 2 ) , as well as the tumour invasiveness related gene secreted protein acid rich in cysteine ( SPARC ) in different human glioblastoma cell lines . ^^^ |
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