Cat.No. : CSC-SC004995 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC004995 |
| Description | Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level. |
| Gene | EPHB4 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HEK293 (CHO and other cell types are also available) |
| Stability | Validated for at least 10 passages |
| Application | 1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Size Form | 2 × 10^6 cells / vial |
| Shipping | Dry Ice |
| Storage | Liquid nitrogen |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Gene Name | EPHB4 EPH receptor B4 [ Homo sapiens ] |
| Gene Symbol | EPHB4 |
| Synonyms | EPHB4; EPH receptor B4; EphB4 , HTK; ephrin type-B receptor 4; Tyro11; ephrin receptor EphB4; soluble EPHB4 variant 1; soluble EPHB4 variant 2; soluble EPHB4 variant 3; hepatoma transmembrane kinase; tyrosine-protein kinase TYRO11; tyrosine-protein kinase receptor HTK; HTK; MYK1; TYRO11; |
| Gene ID | 2050 |
| UniProt ID | P54760 |
| mRNA Refseq | BC052804 |
| Chromosome Location | 7q22 |
| Function | ATP binding; ephrin receptor activity; ephrin receptor activity; nucleotide binding; protein binding; protein tyrosine kinase activity; receptor activity; transmembrane receptor protein tyrosine kinase activity; |
| Pathway | Axon guidance, organism-specific biosystem; Axon guidance, conserved biosystem; EPHB forward signaling, organism-specific biosystem; Ephrin B reverse signaling, organism-specific biosystem; EphrinB-EPHB pathway, organism-specific biosystem; |
| MIM | 600011 |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
Malignant proliferation and cervical lymph node metastasis limit the prognosis of oral squamous cell carcinoma (OSCC). Erythropoietin-producing human hepatocyte B4 (EPHB4) regulates a range of tumor functions, including tumorigenesis, cancer cell adhesion, and metastasis. Here, researchers found that EPHB4 is highly expressed in OSCC tissues and is associated with tumor stage and lymph node metastasis, leading to poor prognosis. Cell experiments and a mouse tongue xenograft model further confirmed that high EPHB4 expression promotes OSCC tumor proliferation and metastasis. Co-immunoprecipitation (co-IP) and mass spectrometry analysis showed that EPHB4 can bind to HMGB1 and maintain HMGB1 stability. Downregulation of HMGB1 inhibited OSCC cell proliferation and metastasis and suppressed NF-κB phosphorylation activation, but did not affect EPHB4 expression. These studies reveal the mechanism by which EPHB4 promotes OSCC proliferation and metastasis by activating the HMGB1-mediated NF-κB signaling pathway, which could serve as a novel biomarker or therapeutic target for controlling OSCC metastasis and improving survival.
Here, researchers constructed EPHB4-overexpressing SCC9 and UM1 cells and verified EPHB4 expression through protein and mRNA analysis (Figures 1A and 1B). EPHB4 overexpression significantly enhanced the proliferation and tumorigenicity of SCC9 and UM1 cells (Figures 1C and 1D). Simultaneously, the results showed enhanced migration and invasion abilities of EPHB4-overexpressing cells. The number of cells crossing the chamber semipermeable membrane also significantly increased (Figures 1E and 1F), and the EPHB4-overexpressing cell lines exhibited stronger scratch repair capabilities.
Figure 1. Upregulation of EPHB4 enhances the proliferation, migration and invasion abilities of OSCC cells. (Yi C, et al., 2021)
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