Cat.No. : CSC-DC008717
Host Cell: HEK293 (Hela and other cell types are also available) Validation: Real-Time RCR
| Cat. No. | CSC-DC008717 |
| 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 | LIMK1 |
| 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 | Limk1 LIM-domain containing, protein kinase [ Mus musculus ] |
| Gene Symbol | Limk1 |
| Gene Description | LIM-domain containing, protein kinase |
| Gene ID | 16885 |
| UniProt ID | P53668 |
| mRNA Refseq | NM_010717.2 |
| Protein Refseq | NP_034847.1 |
| Chromosome Location | 5 G2; 5 75.0 cM |
| Function | ATP binding; heat shock protein binding; kinase activity; metal ion binding; nucleotide binding; protein binding; protein heterodimerization activity; protein kinase activity; protein serine/threonine kinase activity; transferase activity; transferase activity, transferring phosphorus-containing groups; zinc ion binding; |
| Pathway | Axon guidance, organism-specific biosystem; Axon guidance, conserved biosystem; Axon guidance, organism-specific biosystem; Developmental Biology, organism-specific biosystem; Fc gamma R-mediated phagocytosis, organism-specific biosystem; Fc gamma R-mediated phagocytosis, conserved biosystem; G13 Signaling Pathway, 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 |
The expression level of LIM kinase 1 (LIMK1) is closely related to the processing of microRNAs (miRNAs). Studies have shown that LIMK1 expression levels are elevated during the progression of various cancers. Here, researchers investigated the interaction between LIMK1 and miR-106a in oral squamous cell carcinoma (OSCC). They found that miR-106a levels were significantly decreased, while LIMK1 expression was significantly increased in OSCC tissues and cell lines. A strong correlation existed between these changes. Knocking down LIMK1 significantly inhibited OSCC cell proliferation and epithelial-mesenchymal transition (EMT). Bioinformatic analysis predicted that LIMK1 is a potential target gene of miR-106a, and luciferase reporter assays confirmed that miR-106a directly targets LIMK1. Introducing miR-106a into OSCC cells had similar effects to silencing LIMK1. Overexpression of LIMK1 in OSCC cells partially reversed the inhibitory effects caused by miR-106a mimics. These studies suggest that miR-106a inhibits OSCC cell proliferation and EMT by directly reducing LIMK1 expression.
To investigate the function of LIMK1 in oral squamous cell carcinoma (OSCC) cells, researchers constructed LIMK1-knockdown SCC4 cells (Figure 1a). BrdU-ELISA results showed that the proliferation of LIMK1-knockdown SCC4 cells was inhibited (Figure 1b). qRT-PCR results showed that the mRNA levels of PCNA, CDK2, CDK4, cyclin D1, and cyclin E1 were decreased, while the mRNA levels of p21 and p27 were increased in LIMK1-knockdown cells (Figure 1c). Furthermore, LIMK1 knockdown significantly enhanced the expression of the epithelial marker E-cadherin and reduced the expression of the mesenchymal markers N-cadherin and vimentin in SCC4 cells (Figure 1d).
Figure 1. The effects of LIMK1 silencing on the proliferation and EMT in OSCC cells. (Shi B, et al., 2019)
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