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Human Polyclonal FIGF Primary Antibody for IHC (p), WB - ABIN967243
Yamada, Nezu, Shimane, Hirata: Molecular cloning of a novel vascular endothelial growth factor, VEGF-D. in Genomics 1997
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Human Polyclonal FIGF Primary Antibody for ELISA, WB - ABIN535227
Tille, Wang, Lipson, McMahon, Ferrara, Zhu, Hicklin, Sleeman, Eriksson, Alitalo, Pepper: Vascular endothelial growth factor (VEGF) receptor-2 signaling mediates VEGF-C(deltaNdeltaC)- and VEGF-A-induced angiogenesis in vitro. in Experimental cell research 2003
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Human Monoclonal FIGF Primary Antibody for WB - ABIN387760
Romero, Friel, Velez Edwards, Kusanovic, Hassan, Mazaki-Tovi, Vaisbuch, Kim, Erez, Chaiworapongsa, Pearce, Bartlett, Salisbury, Anant, Vovis, Lee, Gomez, Behnke, Oyarzun, Tromp, Williams, Menon: A genetic association study of maternal and fetal candidate genes that predispose to preterm prelabor rupture of membranes (PROM). in American journal of obstetrics and gynecology 2010
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Human Monoclonal FIGF Primary Antibody for IHC (p), IHC - ABIN258825
Schimanski, Schlaegel, Jordan, Moehler, Sgourakis, Drescher, Galle, Lang, Gockel: VEGF-D correlates with metastatic disease in gastric cancer patients undergoing surgery. in World journal of surgery 2011
vegfc (show VEGFC Antibodies) and vegfd cooperatively control lymphangiogenesis throughout the embryo, including during the formation of the trunk lymphatic vasculature. Interestingly, we find that vegfd and vegfc (show VEGFC Antibodies) also redundantly drive artery hyperbranching phenotypes observed upon depletion of Flt1 (show FLT1 Antibodies) or Dll4 (show DLL4 Antibodies).
Vegfd can compensate for loss of Vegfc (show VEGFC Antibodies) 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.
lymphangiogenesis is regulated by two distinct proteolytic mechanisms of ligand activation: one in which VEGFC (show VEGFC Antibodies) activation by ADAMTS3 (show Adamts2 Antibodies) and CCBE1 (show CCBE1 Antibodies) spatially and temporally patterns developing lymphatics, and one in which VEGFD activation by a distinct proteolytic mechanism may be stimulated during inflammatory lymphatic growth
This study uncovers a reciprocal relationship between dendrite geometry, the ability to generate nuclear calcium transients in response to synaptic inputs, and the subsequent induction of expression of plasticity-related and dendritic structure-preserving genes. Insufficient nuclear calcium signaling in CA1 (show CA1 Antibodies) hippocampal neurons and, consequently, reduced expression of the nuclear calcium target gene VEGFD.
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 Antibodies) and VEGF-D play critical roles in this process.
Results provided evidence that IL-7 (show IL7 Antibodies)/IL-7R induce VEGF-D upregulation and promote lymphangiogenesis via c-Fos/c-Jun (show JUN Antibodies) pathway in lung cancer.
Epidermal keratinocyte proliferation in vitro was not affected by VEGF-C (show VEGFC Antibodies) or VEGF-D.
Neutrophils contribute to lymphangiogenesis primarily by modulating VEGF-A (show VEGFA Antibodies) bioavailability and bioactivity and, to a lesser extent, secreting VEGF-D. Neutrophils increased VEGF-A (show VEGFA Antibodies) bioavailability and bioactivity via the secretion of MMP9 (show MMP9 Antibodies) and heparanase (show HPSE Antibodies).
Vegf-d deficiency alters the caliber of initial lymphatics in the dermis leading to reduced functional capacity.
no difference in the levels of VEGF-A (show VEGFA Antibodies), VEGF-C (show VEGFC Antibodies), and VEGF-D in pre-eclampsia compared to normotensive pregnant women stratified by HIV status
CXCR4 (show CXCR4 Antibodies), CCR7 (show CCR7 Antibodies), VEGF-C (show VEGFC Antibodies) and VEGF-D expression might have synergistic effects on the lymph node metastasis in patients with cervical cancer.
VEGF-D-induced changes in serine/threonine kinase (show TLK2 Antibodies) mTOR (show FRAP1 Antibodies) shuttling between the cytosol and nucleus and its increased phosphorylation at Ser (show SIGLEC1 Antibodies)-2448, lead us to the conclusion that the observed shift in redox balance is regulated via mTOR (show FRAP1 Antibodies) kinase signalling.
High VEGFD expression is associated with lymphangioleiomyomatosis.
Data show that VEGF-C (show VEGFC Antibodies), VEGF-D, and VEGFR-3 (show FLT4 Antibodies) were expressed in a substantial percentage of breast carcinomas.
High VEGFD expression is associated with angiogenesis and lymphangiogenesis.
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 Antibodies) 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 Antibodies)) may help to determine the prognosis and management of colorectal cancer (CRC (show CALR Antibodies)).
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