AGTRAP CRISPR/Cas9 KO Plasmid (m): sc-419051
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AGTRAP 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 AGTRAP 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 | |
AGTRAP CRISPR/Cas9 KO Plasmid (m) | sc-419051 | 20 µg | $397.00 |
Overview
Agtrap encodes angiotensin II receptor–associated protein (AGTRAP), a membrane-associated regulator that binds AGTR1 and influences receptor trafficking, internalization, and downstream signaling dynamics. Through modulation of angiotensin II–dependent pathways, AGTRAP can impact MAPK/ERK signaling, cellular stress responses, and inflammatory transcriptional programs, linking it to tissue homeostasis in cardiovascular and renal systems. In mouse models, altered Agtrap activity has been used to interrogate mechanisms underlying blood pressure regulation, vascular remodeling, and kidney function. These properties make AGTRAP a useful node for studying GPCR regulation and renin–angiotensin system signaling in physiologically relevant cell types.
AGTRAP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Agtrap gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Agtrap 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 Agtrap 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 AGTRAP protein expression.
This CRISPR knockout system enables efficient generation of Agtrap-deficient cell models for investigation of AGTRAP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Agtrap exon(s) critical for AGTRAP 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 Agtrap genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by AGTRAP CRISPR/Cas9 KO Plasmid (m) and AGTRAP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Agtrap locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by AGTRAP HDR Plasmid (m) and AGTRAP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Agtrap homology arms to support homology-directed repair at defined Agtrap 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.