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Panoply™ Human ACVR2B Knockdown Stable Cell Line

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

Cat. No. :   CSC-DC000218

Host Cell :   HEK293 (Hela and other cell types are also available) Validation :   Real-Time RCR

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Cell Line Information

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Gene Information

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
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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.Figure 1. ACVR2B regulated OGD/R-stimulated HBMEC damage. (Liu D, et al., 2023)

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