Glypican-3/GPC3 Protein, Cynomolgus (HEK293, Fc)

GPC3 is a member of the heparan sulfate proteoglycans (HSPGs), and attaches to the cell surface by a glycosylphosphatidylinositol anchor. GPC3 is overexpressed in hepatocellular carcinoma (HCC) and can be used as a tumor marker for HCC. Membrane GPC3 can interact with several growth factors to promote the binding of growth factors to their receptors. GPC3 can form a complex with Wnt and activates Wnt signaling, leading to the HCC growth. In addition, GPC3 is also involved in the pathogenesis of Simpson-Golabi-Behmel overgrowth syndrome, regulates cell growth, regulates embryonic and fetal development^[1][2][3]. Glypican-3/GPC3 Protein, Cynomolgus (HEK293, Fc) is the recombinant cynomolgus-derived Glypican-3/GPC3 protein, expressed by HEK293 , with C-hFc labeled tag.

GPC3 is a member of the heparan sulfate proteoglycans (HSPGs), and attaches to the cell surface by a glycosylphosphatidylinositol anchor. GPC3 is overexpressed in hepatocellular carcinoma (HCC) and can be used as a tumor marker for HCC. GPC3 plays a role in liver carcinogenesis^[1]. Specifically, Membrane GPC3 can interact with several growth factors (eg: Wnt, Hedgehogs, bone morphogenetic factors, and FGF) to promote the binding of growth factors to their receptors. GPC3 can form a complex with Wnt and activates Wnt signaling, leading to the HCC growth^[2].
In addition, GPC3 can regulate cell growth. GPC3 is highly expressed in mesodermal embryonic tissues, and the deletion of the GPC3 gene is involved in the pathogenesis of Simpson-Golabi-Behmel overgrowth syndrome. The interaction of GPC3 with IGF2 can reduce IGF2-mediated growth in vivo, which indicates that GPC3 negatively regulates embryonic and fetal development. Besides, GPC3 is a negative transcriptional regulator and tumor suppressor that inhibits the growth of breast, ovary, and lung cancer cells^[2][3].
GPC3 has a cleavage site between Arg358 and Ser359, and can be cleaved by Furin protease^[2].

Immobilized Human FGF basic at 2 μg/mL (100 μL/well) can bind Cynomolgus Glypican-3 Fc with a linear range of 1-31 ng/mL.

Cynomolgus

HEK293

C-hFc

XP_005594665.1 (Q25-H559)

102137748  [NCBI]

QPPPPPPDATCHQVRSFFQRLQPGLKWVPETPVPGSDLQVCLPKGPTCCSRKMEEKYQLTARLNMEQLLQSASMELKFLIIQNAAVFQEAFEIVVRHAKNYTNAMFKNNYPSLTPQAFEFVGEFFTDVSLYILGSDINVDDMVNELFDSLFPVIYTQLMNPGLPDSALDINECLRGARRDLKVFGNFPKLIMTQVSKSLQVTRIFLQALNLGIEVINTTDHLKFSKDCGRMLTRMWYCSYCQGLMMVKPCGGYCNVVMQGCMAGVVEIDKYWREYILSLEELVNGMYRIYDMENVLLGLFSTIHDSIQYVQKNAGKLTTTIGKLCAHSQQRQYRSAYYPEDLFIDKKVLKVAHVEHEETLSSRRRELIQKLKSFISFYSALPGYICSHSPVAENDTLCWNGQELVERYSQKAARNGMKNQFNLHELKMKGPEPVVSQIIDKLKHINQLLRTMSVPKGRVLDKNLDEEGFESGDCGDDEDECIGGSGDGMMKVKNQLRFLAELAYDLDVDDVPGNNQQATPKDNEISTFHNLGNVH

Approximately 40 kDa

≥ 90%, as determined by reducing SDS-PAGE.

Lyophilized powder.

Lyophilized a 0.22 μm filtered solution of Tris with Glycine, Arginine and NaCl, pH 7.5. Normally trehalose is added as protectant before lyophilization.
Note: For SPR assay, please replace the buffer. Primary amine components (e.g., Tris, imidazole) can affect protein-coupled chips.

<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 from date of receipt. 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]. Midorikawa Y, et al. Glypican-3, overexpressed in hepatocellular carcinoma, modulates FGF2 and BMP-7 signaling. Int J Cancer. 2003 Feb 10;103(4):455-65.  [Content Brief]

  [2]. Shih TC, et al. Glypican-3: A molecular marker for the detection and treatment of hepatocellular carcinoma. Liver Res. 2020 Dec;4(4):168-172.  [Content Brief]

  [3]. Zhou F, et al. Glypican-3: A promising biomarker for hepatocellular carcinoma diagnosis and treatment. Med Res Rev. 2018 Mar;38(2):741-767.  [Content Brief]