Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : CSC-SC017586
Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x106 frozen cells/vial
| Cat. No. | CSC-SC017586 |
| 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. |
| Target Gene | XPO1 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HEK293 (CHO and other cell types are also available) |
| Host Cell Species | Species varies |
| Applications |
1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Size | 2 × 10^6 cells / vial |
| Stability | Validated for at least 10 passages |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Storage | Liquid nitrogen |
| Shipping | Dry Ice |
| 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. |
| 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 |
| Gene Name | XPO1 exportin 1 (CRM1 homolog, yeast) [ Homo sapiens ] |
| Gene Symbol | XPO1 |
| Synonyms | emb; CRM1; exp1 |
| Gene Description | exportin 1 (CRM1 homolog, yeast) |
| GeneID | 7514 |
| Uni ProtID | B3KWD0 |
| mRNA Refseq | NM_003400.3 |
| Protein Refseq | NP_003391.1 |
| Chromosome Location | 2p15 |
| Function | RNA binding; protein binding; protein domain specific binding; protein transporter activity; transporter activity; |
| Pathway | Canonical NF-kappaB pathway, organism-specific biosystem; Cell Cycle, organism-specific biosystem; Cell Cycle, Mitotic, organism-specific biosystem; Cyclin A/B1 associated events during G2/M transition, organism-specific biosystem; DNA Replication, organism-specific biosystem; Disease, organism-specific biosystem; Downregulation of TGF-beta receptor signaling, organism-specific biosystem; |
| MIM | 602559 |
Increasing evidence indicates that Exportin-1 (XPO1) plays a pivotal role in hepatocellular carcinoma (HCC). However, the specific mechanisms by which XPO1 mediates resistance to sorafenib in HCC remain unclear. Here, researchers demonstrate that XPO1 is highly expressed in HCC and correlates with poor patient survival. Knockdown of XPO1 inhibits HCC cell migration and proliferation while reducing resistance to sorafenib. Mechanistic studies reveal that XPO1 interacts with the C-terminus of NPM1 and maintains sorafenib resistance by mediating the acetylation of NPM1 at the Lys54 residue. Furthermore, XPO1 binds to Vimentin, promoting epithelial-mesenchymal transition (EMT) in sorafenib-resistant cells. Combination therapy with KPT-8602 and sorafenib effectively suppresses tumor growth. These findings highlight the therapeutic value of targeting XPO1 to overcome sorafenib resistance, suggesting that the combination of KPT-8602 and sorafenib may represent a superior treatment strategy.
The NPM1 protein structure comprises a hydrophobic N-terminus, two acidic regions separated by a bipartite nuclear localization signal, and a unique C-terminal domain (Figure 1E). To identify the XPO1-binding site on NPM1, researchers performed immunoprecipitation (IP) assays using cells expressing Flag-XPO1 and one of four NPM1 deletion mutants. The results showed that the fragment containing amino acid residues 119-294 failed to interact with XPO1, indicating that the N-terminal oligomerization domain (amino acid residues 1-119) mediates the interaction with XPO1 (Figure 1F). Correlation analysis of XPO1 and NPM1 expression in the TCGA database revealed a positive correlation between XPO1 and NPM1 expression levels in TCGA hepatocellular carcinoma (HCC) samples (Figure 1G). Furthermore, the researchers generated an XPO1-overexpressing cell line (HepaRG/XPO1-OE). Western blot analysis demonstrated that XPO1 overexpression promoted NPM1 expression (Figure 1H). To investigate whether XPO1 enhances NPM1 stability, the researchers utilized the proteasome inhibitor MG132. Western blot results confirmed that XPO1 stabilized NPM1 expression in the XPO1-overexpressing cell line following treatment with 10 μM MG132 for 12 hours (Figure 1I).
Figure 1. XPO1 interacts with NPM1. (Wang Z, et al., 2023)
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