Vegfa (NM_009505) Mouse Recombinant Protein

CAT#: TP723803

Purified recombinant protein of Mouse vascular endothelial growth factor A (Vegfa), transcript variant 2

Specifications

Product Data

• Species: Mouse
• Expression Host: HEK293
• Expression cDNA Clone or AA Sequence:
  Protein Sequence

  Mouse VEGF-164, the region of Ala27-Arg190, from gene Accession# NM_009505.4
• Tag: Tag Free
• Predicted MW: 19.3 kDa
• Concentration: lot specific
• Purity: >98%, as determined by Coomassie stained SDS-PAGE.
• Buffer: 5 mM citric acid, 5 mM NaHPO4, 0.15 M NaCl, pH 4.0
• Bioactivity: The ED50 is 1- 4 ng/ml, corresponding to a specific activity of 0.25 - 1 x 10^6 units/mg, determined by the dose dependent stimulation of HUVEC cells proliferation.
• Endotoxin: Less than 0.01 ng per µg protein as determined by the LAL method
• Storage: Store at -80°C.
• Stability: Unopened vial can be stored between 2°C and 8°C for up to 2 weeks, at -20°C for up to 6 months, or at -70°C or below until the expiration date. Aliquots can be stored between 2°C and 8°C for up to one week and stored at -20°C or colder for up to 3 months. Avoid repeated freeze/thaw cycles.

Reference Data

• RefSeq: NP_033531
• Locus ID: 22339
• UniProt ID: Q00731
• Cytogenetics: 17 22.79 cM
• Refseq Size: 3475
• Refseq ORF: 1107
• Synonyms: V; Veg; Vegf; VEGF12; VEGF16; VEGF18; Vpf
• Summary: This gene is a member of the PDGF/VEGF growth factor family. It encodes a heparin-binding protein, which exists as a disulfide-linked homodimer. This growth factor induces proliferation and migration of vascular endothelial cells, and is essential for both physiological and pathological angiogenesis. Disruption of this gene in mice resulted in abnormal embryonic blood vessel formation. This gene is upregulated in many known tumors and its expression is correlated with tumor stage and progression. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. There is also evidence for alternative translation initiation from upstream non-AUG (CUG) codons resulting in additional isoforms. A recent study showed that a C-terminally extended isoform is produced by use of an alternative in-frame translation termination codon via a stop codon readthrough mechanism, and that this isoform is antiangiogenic. Expression of some isoforms derived from the AUG start codon is regulated by a small upstream open reading frame, which is located within an internal ribosome entry site.[provided by RefSeq, Nov 2015]