Browse our anti-Glypican 3 (GPC3) Antibodies

Human Glypican 3 (GPC3) interaction partners

1. serum level significantly higher in hepatocellular carcinoma patients compared to cirrhosis patients

2. LGR5-induced cells formed tumors with canaliculus-like structures in mice and showed canalicular GPC3 staining

3. Study identified an increased protein expression of GPC3 in a lethal group of patients with refractory cisplatin-resistant testicular germ cell tumors.

4. This report by describing for the first time the wide mutational spectrum of GPC3 could help clinicians and geneticists in interpreting GPC3 variants identified incidentally by high-throughput sequencing technologies and also reinforces the need for functional validation of non-truncating mutations

5. GPC3, MAGE1 and 3 were increased with advanced tumor stage, size, and nodule numbers in Hepatocellular Carcinoma

6. Paternal germline mosaicism for a GPC3 deletion in X-linked Simpson-Golabi-Behmel syndrome.

7. GPC3 might act as a target for immunotherapy, and other molecular markers may become molecular markers for early detection of liver cancer and potential targets for immunotherapy.

8. The areas under the receiver operating curve (AUROC) value, sensitivity and specificity of glypican 3 (GPC3) for hepatoblastoma (HB) pretreatment group versus all controls were all significantly lower than those of alpha-fetoprotein (AFP).

9. GPC3 is operating through an intricate molecular signaling network. From the balance of these interactions, the inhibition of breast metastatic spread induced by GPC3 emerges.

10. Its surface is modified with anti-GPC3 antibody.

11. data suggest that transcriptionally targeted delivery of transgene in HCC cells can be achieved using the GPC3 promoter and this targeting strategy produces limited toxicity to normal liver cells

12. High GPC3 expression is associated with Hepatocellular Carcinoma.

13. High GPC3 expression is associated with Hepatocellular Carcinoma.

14. Study demonstrated that GPC3 expression is inversely associated with glucose metabolism, suggesting that GPC3 may play a role in regulating glucose metabolism in hepatocellular carcinoma.

15. the intravenous injection of SF-PL/siGPC3 into nude mice bearing subcutaneous human HepG2 xenografts effectively inhibited tumor growth and also increased the survival rates of animals. These results revealed the great potential of the PEI-modified liposomal nanomedicine carrying SF and siGPC3 to improve Hepatocellular carcinomatreatment

16. Invasive hepatocellular carcinoma (HCC) samples and HCC cell lines with high metastatic potential exhibited higher MXR7 expression. Overexpression of MXR7 promoted epithelial-mesenchymal transition (EMT) progress, and MXR7 depletion repressed the EMT phenotype. Human MXR7 protein is a mediator of EMT and metastasis in HCC.

17. Overexpression of GPC3 was significantly associated with poor prognosis in patients with hepatocellular carcinoma.

18. These data show that glycanation and convertase maturation are not required for soluble mutant GPC3 to inhibit hepatocellular carcinoma cell proliferation.

19. Data indicate that several microRNAs targeting the oncogenic functions of glypican-3 (GPC3).

20. presence distinguishes aggressive from non-aggressive odontogenic tumors

Mouse (Murine) Glypican 3 (GPC3) interaction partners

1. GPC3 might be an alternative therapeutic target for Hepatocellular carcinoma treatment based on a mouse study where Curcumin suppressed HCC tumor growth through down-regulating GPC3/wnt/beta-catenin signaling pathway.

2. This study provides new insights into the roles of GPC1 and GPC3 in mandibular morphogenesis. GPC3-knockout reduces mandibular growth, but GPC1 does not. These findings along with previous studies indicate that glypicans could be potential therapeutic agents to manage craniosynostosis and associated bony dysmorphology.

3. Data show that notum and glypican-1 and glypican-3 gene expression during colorectal cancer (CRC) development and present evidence to suggest them as potential new biomarkers of CRC pathogenesis.

4. Coupling of pGPC3 to liposomes was essential for effective priming of GPC3-specific CTLs.

5. The expression of GPC-3 was altered by DEN treatment.

6. Data suggest that GPC3 down-regulates hepatocyte proliferation by binding to hedgehog (HH) and down-regulating the HH signaling pathway and binding with CD81, thus making it unavailable to bind to Hhex and causing its nuclear translocation.

7. Finding represents a rare four layer genomic overlap consisting of growth associated quantitative trait locus (QTL), body mass associated Gpc3 gene, highly conserved miRNA gene and mature miRNA seed SNP identified in the lean mouse.

8. Hepatocyte overexpression of GPC3 suppresses hepatocyte proliferation and liver regeneration and alters gene expression profiles.

9. glypican-3 is involved in the recruitment of M2-polarized tumor-associated macrophages in hepatocellular carcinoma

10. GPC3 inhibits the PI3K/Akt anti-apoptotic pathway while it stimulates the p38MAPK stress-activated one in murine mammary adenocarcinoma LM3 cells

11. Gpc3 function in development of Simpson-Golabi-Behmel syndrome is IGF-independent

12. GPC3 knockout mice exhibit alterations in the Wnt signaling pathway, which is also associated with the regulation of cell proliferation

13. Polymorphisms in the 3' untranslated region of Gpc3 are strong candidates for the causal sequence variation and loss-of-function mutations can cause overgrowth and developmental abnormalities.

14. results demonstrate that BMP2-SMAD signaling, modulated by GPC3, inhibits renal branching morphogenesis in vivo

15. Altered hematopoiesis in glypican-3-deficient mice results in decreased osteoclast differentiation and a delay in endochondral ossification.

16. Zhx2 acts as a repressor of Gpc3 in the adult liver. Gpc3 is activated in the regenerating liver in an Afr2-dependent manner.

17. A novel glycosyl phosphatidyl inositol (GPI)-linked proteoglycan, Glypican3 (GPC3, binding to GLUT4 was identified.

18. Glypican-3 regulates migration, adhesion and actin cytoskeleton organization in mammary tumor cells through Wnt signaling modulation.

19. GPC3 acts as a negative regulator of Hedgehog signaling during mammalian development.

20. The heparan sulfate proteoglycan (HSPG) glypican-3 mediates commitment of MC3T3-E1 cells toward osteogenesis.