Cat.No. : CSC-DC011312
Host Cell: HEK293 (Hela and other cell types are also available) Validation: Real-Time RCR
| Cat. No. | CSC-DC011312 |
| 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 | PARP1 |
| 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 | Parp1 poly (ADP-ribose) polymerase family, member 1 [ Mus musculus ] |
| Gene Symbol | Parp1 |
| Synonyms | PARP; PPOL; ARTD1; Adprp; Adprt1; C80510; parp-1; sPARP-1; AI893648; 5830444G22Rik |
| Gene Description | poly (ADP-ribose) polymerase family, member 1 |
| Gene ID | 11545 |
| UniProt ID | Q921K2 |
| mRNA Refseq | NM_007415.2 |
| Protein Refseq | NP_031441.2 |
| Chromosome Location | 1 H5; 1 98.6 cM |
| Function | NAD binding; NAD+ ADP-ribosyltransferase activity; protein N-terminus binding; protein binding; transcription factor binding; |
| Pathway | BER complex, organism-specific biosystem; BER complex, conserved biosystem; Base excision repair, organism-specific biosystem; Base excision repair, conserved biosystem; Downregulation of SMAD2/3:SMAD4 transcriptional activity, organism-specific biosystem; FAS pathway and Stress induction of HSP regulation, organism-specific biosystem; Gene Expression, organism-specific biosystem; |
| 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 |
Lymph node metastasis and distant metastasis are significant limiting factors in the treatment of unresectable locally advanced (stage IIIB) and oligometastatic (stage IVa) lung cancer. Here, researchers found that 3-hydroxybutyrate dehydrogenase 1 (BDH1) is associated with lung cancer proliferation and metastasis. BDH1 expression in both tissue and serum samples was correlated with lung cancer metastasis. Mechanistic studies revealed that the PARP1-mediated AMPK-mTOR signaling pathway plays a crucial role in BDH1-induced autophagy. Activation of the mTOR pathway significantly enhanced the effects of BDH1 on cell proliferation and metastasis. These results were validated by knocking down PARP1 expression. Furthermore, in an H460 xenograft mouse model, in vivo administration of BDH1 effectively promoted tumor growth. These findings not only suggest that BDH1 may serve as a novel biomarker and therapeutic target for lung cancer metastasis but also indicate that the PARP1-mediated AMPK-mTOR signaling pathway may play a key role in BDH1-induced autophagy and lung cancer proliferation and metastasis.
To investigate the role of the PARP1/AMPK/mTOR pathway in lung cancer cell proliferation and metastasis, researchers treated PC-9 cells with rapamycin and performed lentiviral transfection. The results showed that the growth, migration, and invasion abilities of PARP1-knockdown cells were significantly reduced (Figure 1A-C). Conversely, rapamycin reversed the effects caused by PARP1 gene knockdown. Rapamycin significantly enhanced the growth, migration, and invasion abilities of PARP1-knockdown cells. These results indicate that rapamycin treatment reversed the proliferation and migration inhibition caused by PARP1 downregulation. As shown in Figure 1D, after starving PARP1-knockdown cells with Hank's buffer for 4 hours, the expression level of LC3-II in PC-9 cells was significantly decreased, while the expression level of P62 was significantly increased. However, rapamycin treatment reversed the effects of PARP1 gene knockdown. Immunofluorescence and electron microscopy further verified the role of PARP1 in autophagy (Figure 1E). Rapamycin treatment enhanced PARP1-induced autophagy. Therefore, the PARP1/AMPK/mTOR pathway may play an important role in lung cancer cell autophagy.
Figure 1. Effects of PARP1/mTOR/autophagy signalling pathway on lung cancer cell growth, migration and invasion. (Zhang Z, et al., 2023)
If your question is not addressed through these resources, you can fill out the online form below and we will answer your question as soon as possible.
Write a review of your use of Biogene products and services in your research. Your review can help your fellow researchers make informed purchasing decisions.
Our promise to you:
Guaranteed product quality, expert customer support.
24x7 CUSTOMER SERVICE
CONTACT US TO ORDER
Copyright © Creative Biogene. All rights reserved.
