Cat.No. : CSC-DC011786
Host Cell: HEK293 (Hela and other cell types are also available) Validation: Real-Time RCR
| Cat. No. | CSC-DC011786 |
| Description | Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free. |
| Gene | PIK3CG |
| Host Cell | HEK293 (Hela and other cell types are also available) |
| Host Cell Species | Homo sapiens (Human) |
| Stability | Validated for at least 10 passages |
| Application | (1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Size Form | >1 × 10^6 cells / vial |
| Shipping | Dry Ice |
| Storage | Liquid Nitrogen |
| Gene Name | PIK3CG phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma [ Homo sapiens ] |
| Gene Symbol | PIK3CG |
| Synonyms | PI3K; PIK3; PI3CG; PI3Kgamma |
| Gene Description | phosphoinositide-3-kinase, catalytic, gamma polypeptide |
| Gene ID | 5294 |
| UniProt ID | P48736 |
| mRNA Refseq | NM_002649.2 |
| Protein Refseq | NP_002640.2 |
| Chromosome Location | 7q22.3 |
| Function | 1-phosphatidylinositol-3-kinase activity; ATP binding; ephrin receptor binding; phosphatidylinositol 3-kinase activity; phosphatidylinositol-4,5-bisphosphate 3-kinase activity; protein binding; protein kinase activity; protein serine/threonine kinase activity; |
| Pathway | 3-phosphoinositide biosynthesis, organism-specific biosystem; 3-phosphoinositide biosynthesis, conserved biosystem; AMPK signaling, organism-specific biosystem; Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; Aldosterone-regulated sodium reabsorption, organism-specific biosystem; Aldosterone-regulated sodium reabsorption, conserved biosystem; |
| MIM | 601232 |
| 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 |
Due to the limited efficacy of current treatments, more effective therapies are urgently needed for ischemic stroke. Here, differential expression analysis and clinical testing showed that PIK3CG is highly expressed in stroke patients. Prolonged oxygen glucose deprivation/reperfusion (OGD/R) exposure increased PIK3CG levels, inhibited cell proliferation, and induced apoptosis. KEGG pathway analysis indicated that PIK3CG is involved in the autophagy pathway. Knockdown of PIK3CG inhibited OGD/R-induced reduction in cell proliferation and OGD/R-induced increases in apoptosis and Beclin 1 and LC3 II expression. After OGD/R, AMPK phosphorylation was upregulated, while mammalian target of rapamycin (mTOR) phosphorylation was downregulated, indicating activation of the AMPK/mTOR autophagy pathway. Knockdown of PIK3CG inhibited metformin-induced increases in Beclin 1, LC3 II, and apoptosis, as well as the reduction in cell proliferation. These results suggest that PIK3CG knockdown protects neuronal cells by inhibiting the AMPK/mTOR autophagy pathway and further suppressing autophagy.
KEGG pathway analysis of differentially expressed genes showed that PIK3CG expression was closely related to the autophagy pathway (Figure 1A-B). After OGD/R treatment of SH-SY5Y cells, Western blot results showed that the expression levels of autophagy-related proteins Beclin 1 and LC3 II (14 kDa) were increased compared to control cells (Figure 1C), indicating that autophagy was activated. Here, researchers constructed PIK3CG knockdown SH-SY5Y cells (Figure 1D). Western blot results showed that the expression of Beclin 1 and LC3 II was decreased in PIK3CG knockdown cells (Figure 1E), indicating that OGD/R-induced autophagy was inhibited. CCK8 assay results showed that compared to the control group, cell viability was decreased after OGD/R treatment, while PIK3CG knockdown partially reversed this decrease (Figure 1F). This indicates that PIK3CG knockdown effectively mitigated the decrease in cell survival induced by OGD/R. Flow cytometry results showed that OGD/R significantly increased the number of apoptotic cells, while PIK3CG knockdown significantly inhibited this increase (Figure 1G). These results indicate that PIK3CG knockdown inhibited OGD/R-induced apoptosis.
Figure 1. The effect of PIK3CG knockdown on autophagy. (Lv L, et al., 2025)
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