VEGF-A (VEGF188) Mouse Protein

Specifications

Product Data
Species	Mouse
Expression Host	E. coli
Expression cDNA Clone or AA Sequence	Protein Sequence (showhide) APTTEGEQKS HEVIKFMDVY QRSYCRPIET LVDIFQEYPD EIEYIFKPSC VPLMRCAGCC NDEALECVPT SESNITMQIM RIKPHQSQHI GEMSFLQHSR CECRPKKDRT KPEKKSVRGK GKGQKRKKKS RFKSWSVHCE PCSERRKHLF VQDPQTCKCS CKNTDSRCKA RQLELNERTC RCDKPRR
Predicted MW	44.2 kDa
Purity	>95% by SDS-PAGE and silver stain
Buffer	Presentation State: Purified State: Lyophilized protein Buffer System: 50 mM Acetic Acid Stabilizer: None
Preparation	Lyophilized protein
Protein Description	Recombinant Murine Vascular Endothelial Growth Factor188. Result by N-terminal sequencing: APTTEGE
Note	Protein RefSeq: NP 001020421 mRNA RefSeq: NM 001025250
Storage	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.
Stability	Shelf life: one year from despatch.
Bioactivity	Biological: Determined by the dose-dependent stimulation of the proliferation of human umbilical vein endothelial cells (HUVEC) using a concentration range of 2-20 ng/ml.
Endotoxin	< 0.1 ng/µg of VEGF188
Reference Data
RefSeq	NP_001020421
Locus ID	22339
UniProt ID	Q00731
Cytogenetics	17 22.79 cM
Synonyms	VEGFA, VEGF, VPF, Vascular endothelial growth factor A, Vascular permeability factor
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]

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