Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : CSC-DC000218
Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR
| Cat. No. | CSC-DC000218 |
| 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. |
| Target Gene | ACVR2B |
| Host Cell | HEK293 (Hela and other cell types are also available) |
| Host Cell Species | Homo sapiens (Human) |
| Applications |
(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models |
| Size | >1 × 106 cells / vial |
| Stability | Validated for at least 10 passages |
| Validation | Real-Time RCR |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Storage | Liquid Nitrogen |
| Shipping | Dry Ice |
| 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 | ACVR2B activin A receptor, type IIB [ Homo sapiens ] |
| Gene Symbol | ACVR2B |
| Synonyms | HTX4; ACTRIIB; ActR-IIB |
| Gene Description | activin A receptor, type IIB |
| Gene ID | 93 |
| Uni Prot ID | Q13705 |
| m RNA Refseq | NM_001106.3 |
| Protein Refseq | NP_001097.2 |
| Chromosome Location | 3p22 |
| Function | ATP binding; activin binding; contributes_to activin receptor activity, type II; growth factor binding; metal ion binding; protein binding; protein serine/threonine kinase activity; protein serine/threonine kinase activity; protein serine/threonine/tyrosine kinase activity; receptor signaling protein serine/threonine kinase activity; transforming growth factor beta-activated receptor activity; |
| Pathway | Cytokine-cytokine receptor interaction, organism-specific biosystem; Cytokine-cytokine receptor interaction, conserved biosystem; Developmental Biology, organism-specific biosystem; Regulation of Signaling by NODAL, organism-specific biosystem; Signal Transduction, organism-specific biosystem; Signaling by BMP, organism-specific biosystem; Signaling by NODAL, organism-specific biosystem; |
| MIM | 602730 |
Circular RNAs (circRNAs) play regulatory roles in cerebrovascular disease. Human brain microvascular endothelial cells (HBMECs) are involved in cerebrovascular dysfunction in ischemic stroke. Here, researchers investigated the role of circ_0000566 in oxygen-glucose deprivation/reoxygenation (OGD/R)-induced HBMECs. Results showed that circ_0000566 and ACVR2B were highly expressed, whereas miR-18a-5p was downregulated in OGD/R-treated HBMECs. OGD/R treatment promoted apoptosis and inflammation in HBMECs and inhibited cell viability, whereas silencing circ_0000566 mitigated these effects. Circ_0000566, acting as a sponge for miR-18a-5p, was involved in OGD/R-induced HBMEC damage. ACVR2B is a direct target of miR-18a-5p. ACVR2B overexpression may abrogate the inhibitory effect of miR-18a-5p on OGD/R-treated HBMECs injury. Circ_0000566 sponged miR-18a-5p to regulate OGD/R-induced HBMECs injury via regulating ACVR2B expression.
Here, researchers investigated the role of ACVR2B in OGD/R-induced HBMEC injury. Transfection of HBMECs with si-ACVR2B significantly reduced ACVR2B protein expression (Figure 1A). Furthermore, OGD/R-induced ACVR2B expression was inhibited by si-ACVR2B transfection (Figure 1B). ACVR2B knockdown in OGD/R-induced HBMECs increased cell viability and Bcl-2 protein levels, while inhibiting LDH release, apoptosis rate, and protein expression of Bax, c-caspase 3, and c-caspase 9 (Figures 1C-J). Furthermore, ACVR2B knockdown also reduced IL-1β, IL-6, and TNF-α levels in OGD/R-induced HBMECs (Figures 1K-M). These data confirm that ACVR2B knockdown alleviates OGD/R-induced HBMEC injury.
Figure 1. ACVR2B regulated OGD/R-stimulated HBMEC damage. (Liu D, et al., 2023)
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