α1B-AR CRISPR/Cas9 KO Plasmid (m): sc-419020
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α1B-AR CRISPR/Cas9 Knockout (KO) Plasmid (m) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the α1B-AR genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α1B-AR CRISPR/Cas9 KO Plasmid (m) | sc-419020 | 20 µg | $397.00 |
Overview
Adra1b encodes the mouse α1B-AR, a G protein–coupled receptor that preferentially couples to Gq/11 to stimulate phospholipase Cβ signaling, increasing IP3-mediated Ca2+ release and diacylglycerol-dependent PKC activation. Through these pathways, α1B-AR regulates smooth muscle tone, neurotransmission, and cellular excitability, and can engage downstream MAPK/ERK programs that influence gene expression and adaptive responses. In neural and cardiovascular contexts, adrenergic receptor signaling intersects with stress-response circuitry and autonomic regulation, linking Adra1b to phenotypes relevant to hypertension, neuropsychiatric traits, and adrenergic dysregulation in disease models. Dissecting α1B-AR function supports mechanistic studies of GPCR signaling bias, receptor cross-talk, and calcium-dependent transcriptional control.
α1B-AR CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Adra1b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adra1b together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the Adra1b open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish α1B-AR protein expression.
This CRISPR knockout system enables efficient generation of Adra1b-deficient cell models for investigation of α1B-AR signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adra1b exon(s) critical for α1B-AR function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple Adra1b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by α1B-AR CRISPR/Cas9 KO Plasmid (m) and α1B-AR CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adra1b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by α1B-AR HDR Plasmid (m) and α1B-AR HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adra1b homology arms to support homology-directed repair at defined Adra1b target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.