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Glypican 3 (GPC3) Antibody (Center)
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IF, WB, E |
|---|---|
| Primary Accession | P51654 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 65563 Da |
| Antigen Region | 335-365 aa |
| Gene ID | 2719 |
|---|---|
| Other Names | Glypican-3, GTR2-2, Intestinal protein OCI-5, MXR7, Secreted glypican-3, GPC3, OCI5 |
| Target/Specificity | This Glypican 3 (GPC3) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 335-365 amino acids from the Central region of human Glypican 3 (GPC3). |
| Dilution | IF~~Tested WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Glypican 3 (GPC3) Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | GPC3 |
|---|---|
| Synonyms | OCI5 |
| Function | Cell surface proteoglycan (PubMed:14610063). Negatively regulates the hedgehog signaling pathway when attached via the GPI- anchor to the cell surface by competing with the hedgehog receptor PTC1 for binding to hedgehog proteins (By similarity). Binding to the hedgehog protein SHH triggers internalization of the complex by endocytosis and its subsequent lysosomal degradation (By similarity). Positively regulates the canonical Wnt signaling pathway by binding to the Wnt receptor Frizzled and stimulating the binding of the Frizzled receptor to Wnt ligands (PubMed:16227623, PubMed:24496449). Positively regulates the non-canonical Wnt signaling pathway (By similarity). Binds to CD81 which decreases the availability of free CD81 for binding to the transcriptional repressor HHEX, resulting in nuclear translocation of HHEX and transcriptional repression (By similarity). Inhibits the dipeptidyl peptidase activity of DPP4 (PubMed:17549790). Plays a role in limb patterning and skeletal development by controlling the cellular response to BMP4 (By similarity). Modulates the effects of growth factors BMP2, BMP7 and FGF7 on renal branching morphogenesis (By similarity). Required for coronary vascular development (By similarity). Plays a role in regulating cell movements during gastrulation (By similarity). |
| Cellular Location | Cell membrane; Lipid-anchor, GPI-anchor {ECO:0000250|UniProtKB:P13265}; Extracellular side {ECO:0000250|UniProtKB:P13265} |
| Tissue Location | Detected in placenta (at protein level) (PubMed:32337544). Highly expressed in lung, liver and kidney |
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Provided below are standard protocols that you may find useful for product applications.
Background
GPC3 is a cell surface proteoglycan that bears heparan sulfate. This protein may be involved in the suppression/modulation of growth in the predominantly mesodermal tissues and organs, and may play a role in the modulation of IGF2 interactions with its receptor and thereby modulate its function. Members of the glypican-related integral membrane proteoglycan family contain a core protein anchored to the cytoplasmic membrane via a glycosyl phosphatidylinositol (GPI) linkage. These proteins may play a role in the control of cell division, growth regulation, and tumor predisposition. Deletion mutations in GPC3 are the cause of Simpson-Golabi-Behmel syndrome (SGBS), also known as Simpson dysmorphia syndrome (SDYS). SGBS is a condition characterized by pre- and postnatal overgrowth (gigantism) with visceral and skeletal anomalies.
References
Nakatsura, T., et al., Clin. Cancer Res. 10(19):6612-6621 (2004).
Boily, G., et al., Br. J. Cancer 90(8):1606-1611 (2004).
Wichert, A., et al., Oncogene 23(4):945-955 (2004).
Midorikawa, Y., et al., Int. J. Cancer 103(4):455-465 (2003).
Sung, Y.K., et al., Cancer Sci. 94(3):259-262 (2003).
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