Angiopoietin-1 Protein, Human (HEK293, Fc)

Angiopoietin-1 Protein, Human (HEK 293, Fc) is a secreted protein located on the outside of cell membranes and is an agonistic ligand of receptor tyrosine kinase that is mainly expressed by vascular endothelial cells and hematopoietic cells. Angiopoietin-1 Protein, Human (HEK 293, Fc) is a potent inducer of sprouting angiogenesis, proming for research of colorectal cancer liver metastases (CRCLMs). Angiopoietin-1 Protein, Human (HEK 293, Fc) induces vascular remodeling through highly organized angiogenesis and tightening of endothelial cell (EC) junctions. Angiopoietin-1 Protein, Human (HEK 293, Fc) regulates angiogenesis, endothelial cell survival, proliferation, migration, adhesion and maintenance of vascular quiescence. Angiopoietin-1 Protein, Human (HEK 293, Fc) is a recombinant protein with a Fc label that consisting of 498 amino acids and is expressed in HEK293 cells^{[1][2][3][4][5][6][7]}.

Angiopoietin-1 Protein, Human (HEK 293, Fc) is a secreted protein ligand for ‘tunica interna endothelial cell kinase’, Tek (Tie2), which is primarily expressed in growing vascular ECs and a subset of hematopoietic cells^[1].
Angiopoietin-1 Protein, Human (HEK 293, Fc) induces distinct angiogenesis through both vascular Tie2 and integrin signaling and nonvascular integrin signaling. Angiopoietin-1 Protein is a potential growth factor for therapeutic angiogenesis and vascular stabilization^[1].
Angiopoietin-1 Protein, Human (HEK 293, Fc) contains a carboxyl-terminal fibrinogen-like domain that binds to the Tie2 receptor, a central coiled-coil domain that enables oligomerization of these fibrinogen-like domains and a short amino-terminal domain that superclusters the oligomers into variably sizedmultimers^[2].
Angiopoietin-1 Protein, Human (HEK 293, Fc) (0.5-10 nM) induces the formation of capillary sprouts in a dose-dependent manner that is completely inhibited by soluble Tie2 receptor extracellular domains in human umbilical vein endothelial cells^[4].
Both the human and mouse Angiopoietin-1 cDNA clones reveals open reading frames encoding 498 amino acids and sharing 97.6% identity^[5].
Angiopoietin-1 Protein, Human (HEK 293, Fc) promotes TKI-resistance via activation of JAK/STAT5 pathway in chronic myeloid leukemia^[7].

Angiopoietin-1 Protein, Human (HEK 293, Fc) (220 ng/mL) induces the formation of capillary sprouts synergied with VEGF (1 ng/mL) in a dose-dependent manner that is completely inhibited by soluble Tie2 receptor extracellular domains in human umbilical vein endothelial cells^[4].
Angiopoietin-1 Protein, Human (HEK 293, Fc) (0-74 ng/mL, 3 days) possesses only very weak mitogenic activity for human umbilical vein endothelial cells^[4].
Angiopoietin-1 Protein, Human (HEK 293, Fc) induces tyrosine phosphorylation of TIE2 in human endothelial cell types (HUCEC, HAEC, HMVEC and HUVEC) and this induction is blocked by the addition of excess soluble TIE2-Fc but not TrkB-Fc^[5].
Angiopoietin-1 Protein, Human (HEK 293, Fc) (0.2 μM, 24 h) acts as a positive regulator of ARP2/3 expression through Tie2-PI3K/AKT pathway in MC38, SW620 and COLO320DM cancer cells^[6].

Overexpression of Angiopoietin-1 Protein, Human (HEK 293, Fc) results in a dramatic increase in the number, size and branching pattern of blood vessels in mice^[3].
Transgenic mice overexpressing Angiopoietin-1 Protein, Human (HEK 293, Fc) has many more large blood vessels in the skin of newborn mice and becomes markedly redder than normal in the skin of older mice^[3].

Measured by the ability of the immobilized protein to support the adhesion of HUVEC human umbilical vein endothelial cells. The ED₅₀ for this effect is ≤356.9 ng/ml, corresponding to a specific activity is ≥2801.905 units/mg.

• 
  Measured by the ability of the immobilized protein to support the adhesion of HUVEC human umbilical vein endothelial cells. The ED₅₀ for this effect is 356.9 ng/ml, corresponding to a specific activity is 2801.905 units/mg.

Human

HEK293

N-hFc

Q15389 (D256-F498)

284  [NCBI]

DTVHNLVNLCTKEGVLLKGGKREEEKPFRDCADVYQAGFNKSGIYTIYINNMPEPKKVFCNMDVNGGGWTVIQHREDGSLDFQRGWKEYKMGFGNPSGEYWLGNEFIFAITSQRQYMLRIELMDWEGNRAYSQYDRFHIGNEKQNYRLYLKGHTGTAGKQSSLILHGADFSTKDADNDNCMCKCALMLTGGWWFDACGPSNLNGMFYTAGQNHGKLNGIKWHYFKGPSYSLRSTTMMIRPLDF

Approximately 57.25-60 kDa due to the glycosylation.

• 
  Greater than 95% as determined by reducing SDS-PAGE.

Lyophilized powder

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4 or PBS, pH 7.4, 5% trehalose, 5% mannitol and 0.01% Tween80 or PBS, pH 7.4, 8% trehalose.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Gou Young Koh, et al. Orchestral actions of angiopoietin-1 in vascular regeneration. Trends Mol Med. 2013 Jan;19(1):31-9.  [Content Brief]

  [2]. Nuri Oh, et al. A Designed Angiopoietin-1 Variant, Dimeric CMP-Ang1 Activates Tie2 and Stimulates Angiogenesis and Vascular Stabilization in N-glycan Dependent Manner.Sci Rep. 2015 Oct 19;5:15291.  [Content Brief]

  [3]. Suri C, et al. Increased vascularization in mice overexpressing angiopoietin-1. Science. 1998 Oct 16;282(5388):468-71.  [Content Brief]

  [4]. Koblizek TI, et al. Angiopoietin-1 induces sprouting angiogenesis in vitro. Curr Biol. 1998 Apr 23;8(9):529-32.  [Content Brief]

  [5]. Davis S, et al. Isolation of angiopoietin-1, a ligand for the TIE2 receptor, by secretion-trap expression cloning. Cell. 1996 Dec 27;87(7):1161-9.  [Content Brief]

  [6]. Rada M, et al. Angiopoietin-1 Upregulates Cancer Cell Motility in Colorectal Cancer Liver Metastases through Actin-Related Protein 2/3. Cancers (Basel). 2022 May 21;14(10):2540.  [Content Brief]

  [7]. Ma D, et al. Intracellular angiopoietin-1 promotes TKI-resistance via activation of JAK/STAT5 pathway in chronic myeloid leukemia. Oncogene. 2023 Jan;42(2):124-137.  [Content Brief]