Cat.No. : CSC-SC012694 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC012694 |
| 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 | PTPN1 |
| 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 | PTPN1 protein tyrosine phosphatase, non-receptor type 1 [ Homo sapiens ] |
| Gene Symbol | PTPN1 |
| Synonyms | PTP1B |
| Gene Description | protein tyrosine phosphatase, non-receptor type 1 |
| Gene ID | 5770 |
| UniProt ID | A8K3M3 |
| mRNA Refseq | NM_002827.2 |
| Protein Refseq | NP_002818.1 |
| Chromosome Location | 20q13.1-q13.2 |
| Pathway | Adherens junction, organism-specific biosystem; Adherens junction, conserved biosystem; Calcineurin-regulated NFAT-dependent transcription in lymphocytes, organism-specific biosystem; Cytokine Signaling in Immune system, organism-specific biosystem; EGF receptor (ErbB1) signaling pathway, organism-specific biosystem; Growth hormone receptor signaling, organism-specific biosystem; Hemostasis, organism-specific biosystem; |
| MIM | 176885 |
| 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 |
Metabolic-associated fatty liver disease (MAFLD) is the most common chronic liver disease globally, characterized by excessive lipid accumulation. Insulin resistance (IR) is a fundamental pathogenic factor in MAFLD. However, there are currently no approved specific therapeutic drugs. Farnesol is a novel compound with antioxidant and anti-inflammatory effects that has recently attracted attention for its hepatoprotective properties. Here, researchers used network pharmacology to predict that protein tyrosine phosphatase non-receptor type 1 (PTPN1) might be a potential target of farnesol in the liver. Subsequently, they found that farnesol improved insulin sensitivity and glucose tolerance in MAFLD mice. Furthermore, farnesol alleviated lipid accumulation by binding to PTPN1 and reducing the dephosphorylation of the insulin receptor (INSR) in HepG2 cells and MAFLD mice. Consequently, the phosphatidylinositol 3-kinase/serine/threonine protein kinase (PI3K/AKT) signaling pathway was activated, leading to decreased levels of downstream proteins. In summary, these studies demonstrate that farnesol alleviates insulin resistance and hepatic steatosis in MAFLD by targeting PTPN1.
To elucidate the precise mechanism by which farrerol reduces lipid accumulation in hepatocytes, researchers conducted experiments using HepG2 cells. The results showed that farrerol supplementation reduced PAOA-induced lipid accumulation in HepG2 cells (Figure 1A). Furthermore, consistent with these results, PTPN1-overexpressing HepG2 cells exhibited more severe lipid accumulation under PAOA stimulation compared to the control group. Subsequent Western blot analysis results were consistent with the above findings, indicating that farrerol significantly increased the phosphorylation levels of INSR and PI3K-AKT, thereby restoring the insulin signaling pathway. However, it is noteworthy that this protective effect was abolished in PTPN1-overexpressing cells (Figure 1B-G). Therefore, farrerol exerts its effect of reducing PAOA-induced lipid droplet accumulation in HepG2 cells by interacting with PTPN1.
Figure 1. Farrerol reduces lipid accumulation in HepG2 cells treated with PAOA. (Gao J, et al., 2024)
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