PLGF (PGF) Rabbit Polyclonal Antibody

Specifications

Product Data
Applications	ELISA, IF, WB
Recommend Dilution	Western Blot: 10 µg/ml, it will detect 25-50 ng/lane of recombinant Human PlGF-1 and PlGF-2 under reducing conditions. Dimers are detected at higher protein amounts/lane. ELISA: 1-5 µg/ml, allows the detection of 1.0-2.5 ng/well of recombinant Human PlGF-1 and PlGF-2. Immunofluorescence/Immunohistochemistry: 5-25 µg/ml, allows the detection of PlGF protein in different Human tissue including placenta and brain tumours.
Reactivity	Human
Host	Rabbit
Clonality	Polyclonal
Immunogen	N-terminal 20 amino acid peptide of native Human PIGF (Leu19 - Val38) produced in Insect Cells.
Specificity	The antibody will react with all Human PlGF isoforms.
Formulation	PBS, pH 7.4 without preservatives State: Purified State: Lyophilized purified Ig fraction
Reconstitution Method	Restore in sterile water to a concentration of 0.1-1.0 mg/ml.
Purification	Affinity Chromatography on Protein A
Conjugation	Unconjugated
Storage Condition	Store lyophilized at 2-8°C for 6 months or at -20°C long term. After reconstitution store the antibody undiluted at 2-8°C for one month or (in aliquots) at -20°C long term. Avoid repeated freezing and thawing.
Gene Name	placental growth factor
Database Link	Entrez Gene 5228 Human UniProt ID P49763
Background	Placenta growth factor (PlGF) is a member of the PDGF/VEGF family of growth factors that share a conserved pattern of eight cysteines. Alternate splicing results in at least three human mature PlGF forms containing 131 (PlGF1), 152 (PlGF2), and 203 (PlGF3) amino acids (aa) respectively. Only PlGF2 contains a highly basic heparinbinding 21 aa insert at the C-terminus. In the mouse, only one P lGF that is the equivalent of human PlGF2 has been identified. Human PlGF1 shares 56%, 55%, 74% and 95% aa identity with the appropriate isoform of mouse, rat, canine and equine PlGF. PlGF is mainly found as variably glycosylated, secreted, 55 - 60 kDa disulfide linked homodimers. Mammalian cells expressing PlGF include villous trophoblasts, decidual cells, erythroblasts, keratinocytes and some endothelial cells. Circulating PlGF increases during pregnancy, reaching a peak in mid-gestation; this increase is attenuated in preeclampsia. However, deletion of PlGF in the mouse does not affect development or reproduction. Postnatally, mice lacking PlGF show impaired angiogenesis in response to ischemia. PlGF binds and signals through VEGF R1/Flt1, but not VEGF R2/Flk-1/KDR, while VEGF binds both but signals only through the angiogenic receptor, VEGF R2. PlGF and VEGF therefore compete for binding to VEGF R1, allowing high PlGF to discourage VEGF/VEGF R1 binding and promote VEGF/VEGF R2mediated angiogenesis. However, PlGF (especially PlGF1) and some forms of VEGF can form dimers that decrease the angiogenic effect of VEGF on VEGF R2. PlGF2, but not PLGF-1, shows heparindependent binding of neuropilin (Npn)-1 and Npn2. PlGF induces monocyte activation, migration, and production of inflammatory cytokines and VEGF. These activities facilitate wound and bone fracture healing, but also contribute to inflammation in active sickle cell disease and atherosclerosis.
Synonyms	PGFL, PLGF, PlGF
Reference Data

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