Cat.No. : CSC-SC008806 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC008806 |
| 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 | LPAR1 |
| 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 | LPAR1 lysophosphatidic acid receptor 1 [ Homo sapiens ] |
| Gene Symbol | EDG2 |
| Synonyms | EDG2; LPA1; VZG1; GPR26; edg-2; vzg-1; Gpcr26; Mrec1.3; rec.1.3 |
| Gene Description | endothelial differentiation, lysophosphatidic acid G-protein-coupled receptor, 2 |
| Gene ID | 1902 |
| UniProt ID | Q5VZX0 |
| mRNA Refseq | NM_057159.2 |
| Protein Refseq | NP_476500.1 |
| Chromosome Location | 9q31.3 |
| Function | G-protein alpha-subunit binding; G-protein coupled receptor activity; PDZ domain binding; lysophosphatidic acid receptor activity; phospholipid binding; protein binding; |
| Pathway | Class A/1 (Rhodopsin-like receptors), organism-specific biosystem; G alpha (i) signalling events, organism-specific biosystem; G alpha (q) signalling events, organism-specific biosystem; GPCR downstream signaling, organism-specific biosystem; GPCR ligand binding, organism-specific biosystem; Gap junction, organism-specific biosystem; Gap junction, conserved biosystem; |
| MIM | 602282 |
| 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 |
Here, researchers investigated the role of lysophosphatidic acid receptor 1 (LPAR1) and its interaction with the PI3K/AKT pathway in the development of intratumoral heterogeneity (ITH) in ovarian serous cystadenocarcinoma (OSC). LPAR1 staining showed significantly higher H values in lymph node metastases and recurrent lesions compared with primary lesions within the same patient. High LPAR1 expression was associated with poor progression-free and overall survival. LPAR1-silenced cells exhibited reduced biological functions in vitro, including invasion, migration, and proliferation, as well as reduced tumor formation in vivo. These functions were significantly enhanced in LPAR1-overexpressing cells both in vitro and in vivo. p-PI3K and p-AKT levels were significantly reduced in LPAR1-knockdown cells, whereas they were significantly increased in LPAR1-overexpressing cells. These studies suggest that LPAR1 plays a crucial role in the invasion, migration, and proliferation of heterogeneous subsets of OSC cell lines, as well as in the development of ITH in OSC, potentially by regulating the activity of the PI3K/AKT pathway.
Transwell invasion/migration assays showed (Figure 1a) that the invasion and migration abilities of LPAR1 knockdown cells were significantly reduced compared with the corresponding control groups. However, the invasion/migration abilities of LPAR1 overexpressing cells were significantly enhanced compared with the corresponding control groups. A cell proliferation assay using a CCK-8 assay was performed to examine the effect of LPAR1 on cell proliferation (Figure 1b). Cell growth curves showed that LPAR1 knockdown inhibited the proliferation of A-Lv-shLPAR1 and S-Lv-shLPAR1 cells. Conversely, LPAR1 overexpression promoted the proliferation of A-Lv-LPAR1 and S-Lv-LPAR1 cells. Furthermore, there were no differences in invasion, migration, or proliferation between the control group and the corresponding wild-type group. The researchers also investigated the correlation between LPAR1 expression and the PI3K/AKT pathway. Western blot analysis revealed that p-PI3K and p-AKT levels were significantly decreased in LPAR1 knockdown cells compared with the control group, whereas they were significantly increased in LPAR1 overexpressing cells (Figure 1c).
Figure 1. Role of LPAR1 in modulating biological functions and the correlation between LPAR1 expression and the PI3K/AKT pathway. (Cui R, et al., 2019)
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