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Panoply™ Human CHEK1 Over-expressing Stable Cell Line

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

Cat. No. :   CSC-SC003082

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

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Gene Information

Cat. No. CSC-SC003082
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 CHEK1
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 CHEK1 checkpoint kinase 1 [ Homo sapiens ]
Gene Symbol CHEK1
Synonyms CHK1
Gene ID 1111
Uni Prot ID B4DT73
m RNA Refseq NM_001114121.2
Protein Refseq NP_001107593.1
Chromosome Location 11q24.2
Function ATP binding; histone kinase activity (H3-T11 specific); protein binding; protein serine/threonine kinase activity;
Pathway Activation of ATR in response to replication stress, organism-specific biosystem; Cell Cycle, organism-specific biosystem; Cell Cycle Checkpoints, organism-specific biosystem; Cell cycle, organism-specific biosystem; Cell cycle, organism-specific biosystem; Cell cycle, conserved biosystem; Chk1/Chk2(Cds1) mediated inactivation of Cyclin B:Cdk1 complex, organism-specific biosystem;
MIM 603078
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Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related death. This study aimed to investigate the role of checkpoint kinase 1 (CHEK1) in NSCLC progression and its regulatory relationship with forkhead box protein M1 (FOXM1). The results showed that both FOXM1 and CHEK1 are highly expressed in NSCLC tissues. CHEK1 overexpression promotes NSCLC cell proliferation, while knockdown of CHEK1 inhibits cell proliferation, suppresses epithelial-mesenchymal transition (EMT), and reduces tumor growth in vivo. FOXM1 can directly bind to the CHEK1 promoter, thereby upregulating CHEK1 expression. These findings suggest that CHEK1 and FOXM1 may be potential therapeutic targets for NSCLC.

To investigate whether CHEK1 affects the progression of non-small cell lung cancer (NSCLC), researchers first constructed A549 and H1299 cell lines stably overexpressing CHEK1 (Figures 1A and B). They then examined the expression levels of epithelial-mesenchymal transition (EMT) markers (N-cadherin, E-cadherin, and vimentin) in these two CHEK1-overexpressing cell lines. The results showed that, compared to the control group, N-cadherin was significantly upregulated and E-cadherin was significantly downregulated in CHEK1-overexpressing A549 cells. Compared to the control group, both N-cadherin and vimentin were significantly upregulated in CHEK1-overexpressing H1299 cells (Figures 1C and D). Furthermore, the researchers used Transwell assays to examine the effect of stable CHEK1 overexpression on the migration and invasion abilities of A549 and H1299 cells. As shown in Figures 1E and 1F, the migration and invasion abilities of CHEK1-overexpressing A549 and H1299 cells were significantly enhanced. Next, to investigate whether CHEK1 overexpression regulates the proliferation of non-small cell lung cancer (NSCLC) cells, they assessed the effect of stable CHEK1 overexpression on the survival of A549 and H1299 cells. The results showed that the survival of both CHEK1-overexpressing cell lines was significantly improved (Figure 1G and H). Furthermore, stable CHEK1 overexpression significantly reduced the proportion of cells in S phase (Figure 1I-L).

Figure 1. CHEK1 overexpression promotes the migration and proliferation of NSCLC cells.Figure 1. CHEK1 overexpression promotes the migration and proliferation of NSCLC cells. (Lu X, et al., 2025)

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