Cat.No. : CSC-SC005030 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC005030 |
| 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 | ERBB4 |
| 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 | ERBB4 v-erb-a erythroblastic leukemia viral oncogene homolog 4 (avian) [ Homo sapiens ] |
| Gene Symbol | ERBB4 |
| Synonyms | HER4; p180erbB4 |
| Gene Description | v-erb-a erythroblastic leukemia viral oncogene homolog 4 (avian) |
| Gene ID | 2066 |
| UniProt ID | Q15303 |
| mRNA Refseq | NM_001042599.1 |
| Protein Refseq | NP_001036064.1 |
| Chromosome Location | 2q33.3-q34 |
| Function | ATP binding; epidermal growth factor receptor binding; protein binding; protein homodimerization activity; protein tyrosine kinase activity; receptor signaling protein tyrosine kinase activity; transcription regulatory region DNA binding; transmembrane receptor protein tyrosine kinase activity; |
| Pathway | Adaptive Immune System, organism-specific biosystem; Calcium signaling pathway, organism-specific biosystem; Calcium signaling pathway, conserved biosystem; Constitutive PI3K/AKT Signaling in Cancer, organism-specific biosystem; DAP12 interactions, organism-specific biosystem; DAP12 signaling, organism-specific biosystem; Disease, organism-specific biosystem; |
| MIM | 600543 |
| 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 |
MicroRNAs (miRNAs) are involved in the development and progression of hepatocellular carcinoma (HCC) and can control gene expression by directly targeting or regulating DNA methylation. Here, researchers analyzed the mechanism of miR-93-5p in HCC progression. miR-93-5p abundance was enhanced and ERBB4 level was reduced in HCC tumour tissues of 62 patients and HCC cell lines, in contrast with that in paired normal tissues of 62 patients and normal cell lines. ERBB4 is a target of miR-93-5p. Knockdown of miR-93-5p or overexpression of ERBB4 both inhibited HCC cell proliferation and promoted apoptosis by reducing cell viability and colony formation ability, as well as inducing cell cycle arrest. Silencing ERBB4 attenuated the effects of miR-93-5p knockdown on cell proliferation and apoptosis. In HCC samples and cell lines, the level of ERBB4 promoter DNA methylation was increased, and ERBB4 expression was increased through TETs (TET1, TET2, and TET3). miR-93-5p targets TETs to regulate ERBB4 expression. TET silencing alleviates the effects of miR-93-5p knockdown on cell proliferation and apoptosis. In xenograft models, miR-93-5p knockdown inhibits HCC growth. Therefore, miR-93-5p knockdown inhibits HCC progression by increasing ERBB4 and TETs-dependent DNA demethylation.
To investigate the effects of miR-93-5p and ERBB4 on the progression of hepatocellular carcinoma (HCC) in vitro, researchers transfected Huh-7 and SNU-449 cells with anti-NC, anti-miR-93-5p, vector or ERBB4 overexpression vector. The transfection effect of the ERBB4 overexpression vector is shown in Figure 1A-B. Furthermore, the researchers assessed the effects of miR-93-5p and ERBB4 on the proliferation of Huh-7 and SNU-449 cells by measuring cell viability, colony formation ability, and cell cycle progression. The results showed that cell proliferation was significantly inhibited in miR-93-5p knockdown cells or ERBB4 overexpression cells, manifested as decreased cell viability and colony formation ability, and cell cycle arrest at the G0/G1 phase (Figure 1C-G). In addition, apoptosis was significantly increased in miR-93-5p knockdown cells or ERBB4 overexpression cells (Figure 1H). These results indicate that miR-93-5p knockdown or ERBB4 overexpression has an anti-hepatocellular carcinoma effect.
Figure 1. The influence of miR-93-5p silence or ERBB4 overexpression on cell proliferation and apoptosis. (Li Y, et al., 2021)
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