Cat.No. : CSC-SC016363 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC016363 |
| 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 | TNFRSF1A |
| 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 | TNFRSF1A tumor necrosis factor receptor superfamily, member 1A [ Homo sapiens ] |
| Gene Symbol | TNFRSF1A |
| Synonyms | TNFRSF1A; tumor necrosis factor receptor superfamily, member 1A; TNFR1; tumor necrosis factor receptor superfamily member 1A; CD120a; TNF R; TNF R I; TNF R55; TNFAR; TNFR60; TNF-R1; TNF-RI; TNFR-I; tumor necrosis factor-alpha receptor; tumor necrosis factor receptor type 1; tumor necrosis factor binding protein 1; tumor necrosis factor receptor 1A isoform beta; FPF; p55; p60; TBP1; TNF-R; p55-R; TNFR55; TNF-R-I; TNF-R55; MGC19588; |
| Gene ID | 7132 |
| UniProt ID | P19438 |
| mRNA Refseq | BC010140 |
| Chromosome Location | 12p13.2 |
| Function | protease binding; protein binding; receptor activity |
| Pathway | Adipocytokine signaling pathway, organism-specific biosystem; Adipocytokine signaling pathway, conserved biosystem; Alzheimers disease, organism-specific biosystem; Alzheimers disease, conserved biosystem; Amyotrophic lateral sclerosis (ALS), organism-specific biosystem; Amyotrophic lateral sclerosis (ALS), conserved biosystem; Apoptosis, organism-specific biosystem; |
| MIM | 191190 |
| 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 |
Oxygen-glucose deprivation/reoxygenation (OGD/R)-mediated renal ischemia frequently results in increased apoptosis and heightened inflammation. Sap, a flavonoid extracted from Caesalpinia sappan L., possesses various cytoprotective activities. Here, researchers investigated the effects of Sap on HK-2 cells under OGD/R treatment. The results showed that Sap may be associated with renal ischemia. Furthermore, Sap alleviated OGD/R-mediated HK-2 cell damage by increasing cell viability and inhibiting apoptosis and inflammation. Sap also inhibited the activation of the TNFRSF1A/NF-κB signaling pathway. Moreover, upregulation of TNFRSF1A attenuated the inhibitory effect of Sap on OGD/R-mediated apoptosis and inflammation. In conclusion, Sap alleviates OGD/R-induced HK-2 cell damage by downregulating the TNFRSF1A/NF-κB signaling pathway, thus providing a theoretical basis for the treatment of renal ischemia.
To investigate whether TNFRSF1A overexpression could reverse the inhibitory effect of SAP in HK-2 cells, researchers conducted a rescue experiment. The results showed that in TNFRSF1A-overexpressing HK-2 cells treated with OGD/R and SAP, increased apoptosis rate (Figure 1A), enhanced LDH release (Figure 1B), and increased caspase-3 activity (Figure 1C) reversed the effects of SAP. Furthermore, the results confirmed that, compared to the OGD/R+Sap group, the expression levels of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and IL-18 were significantly increased in TNFRSF1A-overexpressing HK-2 cells (Figures 2A-D). These results demonstrate that SAP alleviated HK-2 cell damage in the OGD/R model in a dose-dependent manner by downregulating TNFRSF1A.
Figure 1. TNFRSF1A overexpression mitigated the suppressive influence of Sap on OGD/R-mediated cell death. (Wang Q, et al., 2022)
Figure 2. TNFRSF1A upregulation lessened the suppressive effect of Sap on OGD/R-mediated inflammation. (Wang Q, et al., 2022)
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