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Human FIGF Protein expressed in Human Cells - ABIN2003050
Stacker, Stenvers, Caesar, Vitali, Domagala, Nice, Roufail, Simpson, Moritz, Karpanen, Alitalo, Achen: Biosynthesis of vascular endothelial growth factor-D involves proteolytic processing which generates non-covalent homodimers. in The Journal of biological chemistry 1999
Show all 4 references for ABIN2003050
Mouse (Murine) FIGF Protein expressed in Human Cells - ABIN2007419
Baldwin, Catimel, Nice, Roufail, Hall, Stenvers, Karkkainen, Alitalo, Stacker, Achen: The specificity of receptor binding by vascular endothelial growth factor-d is different in mouse and man. in The Journal of biological chemistry 2001
Show all 4 references for ABIN2007419
Rat (Rattus) FIGF Protein expressed in Human Cells - ABIN2009160
McColl, Baldwin, Roufail, Freeman, Moritz, Simpson, Alitalo, Stacker, Achen: Plasmin activates the lymphangiogenic growth factors VEGF-C and VEGF-D. in The Journal of experimental medicine 2003
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Human FIGF Protein expressed in Escherichia coli (E. coli) - ABIN1047904
Yamada, Nezu, Shimane, Hirata: Molecular cloning of a novel vascular endothelial growth factor, VEGF-D. in Genomics 1997
Show all 3 references for ABIN1047904
Human FIGF Protein expressed in HEK-293 Cells - ABIN2181913
Leppänen, Jeltsch, Anisimov, Tvorogov, Aho, Kalkkinen, Toivanen, Ylä-Herttuala, Ballmer-Hofer, Alitalo: Structural determinants of vascular endothelial growth factor-D receptor binding and specificity. in Blood 2011
Vegfd can compensate for loss of Vegfc (show VEGFC Proteins) in zebrafish facial lymphatic sprouting.
VEGFD-mediated pathologies include or involve an underlying dysregulation of SOXF-mediated transcriptional networks.
Our studies therefore identified the first non-mammalian VEGF-D and established its in vivo role for vascular system development during vertebrate embryogenesis and provided an alternative animal model to further reveal functions of VEGF-D.
Overexpression of VEGFD causes lymphatic hyperplasia in lung, kidney, and brown adipose tissue. Overexpression of VEGFD in white adipose tissue causes a de novo lymphatic network.
Vegf-d promotes oedema in response to hyperoxia in mice and support the hypothesis that VEGF-D signalling promotes vascular leak in human hyperoxic acute lung injury (HALI).
VEGF-D may be beneficial in early-stage tumors since it suppresses the pro-tumorigenic inflammation, while at later stages VEGF-D-induced tumor lymphatics provide a route for metastasis.
These results suggest that lymph node lymphangiogenesis occurs before metastasis in OSCC. VEGF-A (show VEGFA Proteins) and VEGF-D play critical roles in this process.
Results provided evidence that IL-7 (show IL7 Proteins)/IL-7R induce VEGF-D upregulation and promote lymphangiogenesis via c-Fos/c-Jun (show JUN Proteins) pathway in lung cancer.
Epidermal keratinocyte proliferation in vitro was not affected by VEGF-C (show VEGFC Proteins) or VEGF-D.
Neutrophils contribute to lymphangiogenesis primarily by modulating VEGF-A (show VEGFA Proteins) bioavailability and bioactivity and, to a lesser extent, secreting VEGF-D. Neutrophils increased VEGF-A (show VEGFA Proteins) bioavailability and bioactivity via the secretion of MMP9 (show MMP9 Proteins) and heparanase (show HPSE Proteins).
Vegf-d deficiency alters the caliber of initial lymphatics in the dermis leading to reduced functional capacity.
Vascular endothelial growth factor-C (show VEGFC Proteins) and -D are involved in lymphangiogenesis in mouse unilateral ureteral obstruction.
VEGF-D has a role in progestin-induced break-through bleeding in thin-walled blood and lymphatic endometrial vessels
VEGF-D and its receptors were co-localized on blood vessels in clinical samples of human lungs exposed to hyperoxia; hence, VEGF-D may act directly on blood vessels to promote fluid leak.
VEGF-D-enhanced metastasis was evidently reversed by MP. MP significantly reduced the invasion of VEGFD-SK cells, tumor volume, lymphatic metastasis rates and lymphatic vessel density compared with control groups
Sulf2 (show SULF2 Proteins) facilitated lymphangiogenesis in breast cancer cells by regulating VEGF-D and that the AKT1related signaling pathway was involved.
Data indicate that vascular endothelial growth factor D (VEGF-D) was the best indicator of metastasis and vascular endothelial growth factors and receptor-3 (VEGFR-3 (show FLT4 Proteins)) may help to determine the prognosis and management of colorectal cancer (CRC (show CALR Proteins)).
Taken together, our data suggest that TNF-alpha (show TNF Proteins) can promote lymphangiogenesis and lymphatic metastasis of GBC through the ERK1/2/AP-1 (show FOSB Proteins)/VEGF-D pathway.
VEGF-D may play an important role in the process of lymphatic metastasis of epithelial ovarian cancer
CCL21 (show CCL21 Proteins)/CCR7 (show CCR7 Proteins) induce VEGF-D up-regulation and promote lymphangiogenesis via ERK (show EPHB2 Proteins)/Akt (show AKT1 Proteins) pathway in lung cancer.
The most extensively accepted signaling pathways promoting lymphangiogenesis in tumors include the secreted lymphangiogenic proteins: VEGF-C (show VEGFC Proteins) and VEGF-D, and their cognate receptor on lymphatic endothelium VEGF receptor (show FLT1 Proteins)-3 (VEGFR-3 (show FLT4 Proteins)).
Study demonstrated that VEGF-D upregulates myofibroblast proliferation, migration, and collagen synthesis through activation of VEGF pathway.
MTA1 (show MTA1 Proteins) is up-regulated in CRC (show CALR Proteins); its expression is inversely associated with lymphatic metastases and the expression of VEGFC (show VEGFC Proteins), VEGFD and VEGFR3 (show FLT4 Proteins)
The protein encoded by this gene is a member of the platelet-derived growth factor/vascular endothelial growth factor (PDGF/VEGF) family and is active in angiogenesis, lymphangiogenesis, and endothelial cell growth. This secreted protein undergoes a complex proteolytic maturation, generating multiple processed forms which bind and activate VEGFR-2 and VEGFR-3 receptors. This protein is structurally and functionally similar to vascular endothelial growth factor C. Read-through transcription has been observed between this locus and the upstream PIR (GeneID 8544) locus.
c-fos induced growth factor (vascular endothelial growth factor D)
, vascular endothelial growth factor D
, vascular enthelial growth factor D
, vegf d
, Vascular endothelial growth factor D
, c-fos-induced growth factor