Human PlGF-3 Antibody

Catalog #: MAB7758 Datasheet / COA / SDS

Catalog #	Availability	Size / Price	Qty
MAB7758-100
MAB7758-SP

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Summary Data Examples Preparation and Storage Reconstitution Calculator Background Product Datasheets Related Research Areas

Human PlGF-3 Antibody Summary

Species Reactivity

Human

Specificity

Detects human PIGF-3 in direct ELISAs.

Source

Monoclonal Mouse IgG_2B Clone # 1039018

Purification

Protein A or G purified from hybridoma culture supernatant

Immunogen

Spodoptera frugiperda Sf21 (baculovirus)-derived human PlGF-3
Leu19-Arg221
Accession # P49763

Formulation

Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.

Label

Unconjugated

Applications

Recommended Concentration

Sample

Immunohistochemistry

5-25 µg/mL

Immersion fixed paraffin-embedded sections of human placenta

Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.

Scientific Data

Immunohistochemistry

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PlGF-3 in Human Placenta. PlGF-3 was detected in immersion fixed paraffin-embedded sections of human placenta using Mouse Anti-Human PlGF-3 Monoclonal Antibody (Catalog # MAB7758) at 5 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Mouse IgG VisUCyte™ HRP Polymer Antibody (VC001). Before incubation with the primary antibody, tissue was subjected to heat-induced epitope retrieval using Antigen Retrieval Reagent-Basic (CTS013). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to decidual cells. Staining was performed using our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents.

Reconstitution Calculator

Preparation and Storage

Reconstitution

Reconstitute at 0.5 mg/mL in sterile PBS.

Shipping

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.

Background: PlGF-3

Placenta growth factor (PlGF or PGF) is a member of the PDGF/VEGF family of growth factors that share a conserved pattern of eight cysteines (1‑3). Alternative splicing likely results in four human mature PlGF forms containing 131 (PlGF‑1), 152 (PlGF‑2), 203 (PlGF‑3), or 224 (PlGF-4) amino acids (aa) (1-3). The PlGF-3 form is limited to humans. PlGF-3 and PlGF-1 do not contain a heparin binding insert at the C‑terminus (1, 2). Within the region shared with other PlGF isoforms (aa 18-131), human PlGF‑3 shares 68%, 66%, 96%, 96%, 87% and 77% aa sequence identity with mouse, rat, porcine, equine, canine and bovine PlGF, respectively. PlGF is mainly found as a variably glycosylated, secreted, 55 ‑ 60 kDa, disulfide linked homodimer (1, 4). Mammalian cells expressing all forms of PlGF include villous trophoblasts and decidual cells, with smaller amounts in erythroblasts, keratinocytes and some endothelial cells (1-3, 5, 6). Circulating PlGF increases during pregnancy, reaching a peak in mid‑gestation; this increase is attenuated in preeclampsia (7). However, deletion of PlGF in the mouse, which expresses only PlGF-2, does not affect development or reproduction (3, 8). Postnatally, mice lacking PlGF show impaired angiogenesis in response to ischemia (8). PlGF binds and signals through VEGF R1/Flt‑1 and Neuropilins (some isoforms), but not VEGF R2/Flk‑1/KDR (3, 8-10). In contrast, VEGF binds both VEGF R1 and R2, but signals mainly through the angiogenic receptor, VEGF R2. PlGF and VEGF therefore compete for binding to VEGF R1, resulting in a PlGF inhibition of VEGF/VEGF R1 binding coupled to a subsequent promotion of VEGF/VEGF R2‑mediated angiogenesis (1, 3, 8, 9). However, PlGF (especially PlGF‑1) and some forms of VEGF can form dimers that can alter the angiogenic effect of VEGF on VEGF R2 (3, 4, 9). PlGF induces monocyte activation, migration, and production of inflammatory cytokines and VEGF (3). These activities facilitate wound and bone fracture healing, and also contribute to inflammation in active sickle cell disease and atherosclerosis (5, 6, 8, 11‑14). Circulating PlGF often correlates with tumor stage and aggressiveness (3, 14, 15).

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