Detects mouse VEGF-D in direct ELISAs and Western blots. In direct ELISAs, less than 40% cross-reactivity with recombinant human (rh) VEGF-D is observed, and less than 1% cross-reactivity with recombinant mouse (rm) VEGF115, rmVEGF120, rhVEGF, rhVEGF-B, and rmVEGF165 is observed.
Polyclonal Goat IgG
E. coli-derived recombinant mouse VEGF-D Phe98-Ser206 Accession # P97946
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied as a 0.2 µm filtered solution in PBS.
VEGF-D in Mouse Embryo. VEGF-D was detected in immersion fixed frozen sections of mouse embryo (13 d.p.c.) using Goat Anti-Mouse VEGF‑D Antigen Affinity-purified Polyclonal Antibody (Catalog # AF469) at 15 µg/mL overnight at 4 °C. Tissue was stained using the Anti-Goat HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS008) and counterstained with hematoxylin (blue). Specific staining was localized to seminiferous tubules in testis. View our protocol for Chromogenic IHC Staining of Frozen Tissue Sections.
Preparation and Storage
Reconstitute at 0.2 mg/mL in sterile PBS.
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
Vascular endothelia growth factor D (VEGF-D), also known as c-fos-induced growth factor (FIGF), is a secreted glycoprotein of the VEGF/PDGF family. VEGFs regulate angiogenesis and lymphangiogenesis during development and tumor growth, and are characterized by eight conserved cysteine residues that form a cysteine-knot structure (1‑3). VEGF-C and VEGF-D, which share 23% amino acid (aa) sequence identity, are uniquely expressed as preproproteins that contain long N- and C-terminal propeptide extensions around the VEGF homology domain (VHD) (1, 2). Proteolytic processing of either 358 aa or 326 aa splice forms of mouse VEGF-D preproprotein creates a secreted proprotein. Further processing by extracellular serine proteases, such as plasmin or furin-like proprotein convertases, forms mature VEGF-D consisting of non-covalently linked 42 kDa homodimers of the 117 aa VHD (4‑7). Mature mouse VEGF-D shares 94%, 99%, 93%, 91% and 89% aa identity with the VHD of human, rat, equine, canine and bovine VEGF-D, respectively. It is expressed in adult lung, heart, muscle, and small intestine, and is most abundantly expressed in fetal lungs and skin (1-4). Mouse and human VEGF-D are ligands for VEGF receptor 3 (VEGF-R3, also called Flt-4) that are active across species and show enhanced affinity when processed (8). Unlike human VEGF‑D, which is also a ligand for VEGF-R2 (also called Flk-1 or KDR), mouse VEGF-D does not bind to VEGF-R2 (8). VEGF-R3 is strongly expressed in lymphatic endothelial cells and is essential for regulation of the growth and differentiation of lymphatic endothelium (1, 2). While VEGF-C is the critical ligand for VEGF-R3 during embryonic lymphatic development, VEGF-D is most active in neonatal lymphatic maturation and bone growth (9‑11). Both promote tumor lymphangiogenesis (12). Consonant with their activity on VEGF receptors, binding of VEGF-C and VEGF-D to neuropilins contributes to VEGF-R3 signaling in lymphangiogenesis, while binding to integrin alpha 9 beta 1 mediates endothelial cell adhesion and migration (13, 14).
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The data collected includes not only links to publications in PubMed,
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