Panoply™ Human FAS Over-expressing Stable Cell Line

Name: Panoply™ Human FAS Over-expressing Stable Cell Line
SKU: CSC-SC005538
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CSC-SC005538

Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x10⁶ frozen cells/vial

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Cell Line Information

Cell Culture Information

Safety and Packaging

Gene Information

Cat. No.	CSC-SC005538
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	FAS
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	FAS Fas (TNF receptor superfamily, member 6) [ Homo sapiens ]
Gene Symbol	FAS
Synonyms	FAS; Fas (TNF receptor superfamily, member 6); APT1, FAS1, TNFRSF6, tumor necrosis factor receptor superfamily, member 6; tumor necrosis factor receptor superfamily member 6; APO 1; CD95; Fas AMA; FAS 827dupA; CD95 antigen; FASLG receptor; apoptosis antigen 1; Delta Fas/APO-1/CD95; APO-1 cell surface antigen; apoptosis-mediating surface antigen FAS; tumor necrosis factor receptor superfamily, member 6; APT1; FAS1; APO-1; FASTM; ALPS1A; TNFRSF6;
GeneID	355
Uni ProtID	P25445
mRNA Refseq	BC012479
Chromosome Location	10q24.1
Function	binding; identical protein binding; kinase binding; protein binding; receptor activity; receptor activity; signal transducer activity; transmembrane signaling receptor activity; tumor necrosis factor-activated receptor activity;
Pathway	Activation of Pro-Caspase 8, organism-specific biosystem; Adipogenesis, organism-specific biosystem; African trypanosomiasis, organism-specific biosystem; African trypanosomiasis, conserved biosystem; Allograft rejection, organism-specific biosystem; Allograft rejection, conserved biosystem; Alzheimers disease, organism-specific biosystem;
MIM	134637

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MicroRNA-25 (miR-25) has been reported to be an important miRNA marker in neural cells and is highly expressed in ischemic brain tissue. However, the precise mechanism and role of miR-25 in cerebral ischemia/reperfusion (I/R) injury require further investigation. Here, researchers established an oxygen-glucose deprivation (OGD) model in human SH-SY5Y and IMR-32 cells to mimic I/R injury and evaluated the role of miR-25 in regulating OGD/reperfusion (OGDR)-induced apoptosis. They found that miR-25 was downregulated in the OGDR model. Overexpression of miR-25 via miRNA mimic transfection significantly inhibited OGDR-induced apoptosis. Furthermore, bioinformatics analysis identified Fas as a target gene of miR-25. Dual-luciferase reporter assays confirmed the interaction between miR-25 and the 3′-untranslated region (UTR) of Fas mRNA. In the OGDR model, overexpression of miR-25 led to downregulation of Fas protein expression. Subsequently, small interfering RNA (siRNA)-mediated knockdown of Fas expression also inhibited OGDR-induced cell apoptosis. Conversely, overexpression of Fas abolished the protective effect of miR-25 on OGDR-induced cells. Taken together, these results suggest that upregulation of miR-25 may inhibit cerebral ischemia-reperfusion injury-induced apoptosis by downregulating Fas/FasL, making it a promising therapeutic target.

Here, researchers conducted MTT and caspase-3 assays to investigate the effects of Fas overexpression and silencing on cell viability and caspase-3 activity. In Fas-overexpressing cells, cell viability was reduced to a level comparable to that in the OGDR group (Figure 1a). Conversely, Fas silencing significantly improved cell viability. Figure 1b shows that caspase-3 activity was enhanced in Fas-overexpressing cells but significantly suppressed by Fas silencing. Taken together, these results demonstrate that Fas overexpression significantly inhibits cell survival, even in the absence of OGDR. Furthermore, Fas silencing exhibited the opposite effect, reversing the effects of OGDR treatment.

Figure 1. Fas overexpression inhibited cell survival, whereas Fas silencing promoted cell survival. (Zhang J, et al., 2016)

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