AT1a CRISPR/Cas9 KO Plasmid (m): sc-419048
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AT1a 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 AT1a 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 | |
AT1a CRISPR/Cas9 KO Plasmid (m) | sc-419048 | 20 µg | $397.00 |
Overview
Agtr1a encodes the mouse angiotensin II type 1A receptor (AT1a), a seven-transmembrane GPCR that mediates angiotensin II signaling in vascular, renal, cardiac, and neural tissues. Upon ligand engagement, AT1a couples primarily to Gq/11 to activate phospholipase C, elevate intracellular Ca2+, and stimulate PKC-dependent signaling, while also engaging MAPK/ERK cascades and β-arrestin–linked pathways that influence transcriptional programs. This receptor integrates renin–angiotensin system inputs with cellular processes including vasomotor regulation, sodium and fluid handling, oxidative stress responses, and inflammatory signaling. Dysregulated AT1a pathway activity is widely used as a mechanistic axis in models of hypertension, cardiac hypertrophy and remodeling, kidney injury, and vascular dysfunction, making Agtr1a a common target for pathway dissection in cardiovascular and renal biology.
AT1a CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Agtr1a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Agtr1a 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 Agtr1a 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 AT1a protein expression.
This CRISPR knockout system enables efficient generation of Agtr1a-deficient cell models for investigation of AT1a signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Agtr1a exon(s) critical for AT1a 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 Agtr1a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by AT1a CRISPR/Cas9 KO Plasmid (m) and AT1a CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Agtr1a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by AT1a HDR Plasmid (m) and AT1a HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Agtr1a homology arms to support homology-directed repair at defined Agtr1a 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.