AKAP 7 CRISPR/Cas9 KO Plasmid (h): sc-406308
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AKAP 7 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 AKAP 7 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AKAP 7 Antibody (1F9): sc-517021
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AKAP 7 CRISPR/Cas9 KO Plasmid (h) | sc-406308 | 20 µg | $397.00 |
Overview
AKAP7 (A-kinase anchoring protein 7) is a PKA scaffold that spatially restricts cAMP-dependent signaling by tethering protein kinase A to defined subcellular microdomains. Through compartmentalization of PKA and associated effectors, AKAP7 helps coordinate phosphorylation events that regulate ion channel activity, membrane excitability, and downstream transcriptional programs responsive to cAMP. This anchored signaling contributes to fine control of cellular dynamics such as calcium handling and stimulus-coupled responses in excitable and non-excitable tissues. Dysregulation of cAMP/PKA scaffolding networks, including altered AKAP7-dependent signaling, is relevant to mechanistic studies of cardiac electrophysiology, neuronal signaling, and broader pathologies linked to aberrant kinase compartmentalization.
AKAP 7 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the AKAP7 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the AKAP7 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 AKAP7 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 AKAP 7 protein expression.
This CRISPR knockout system enables efficient generation of AKAP7-deficient cell models for investigation of AKAP 7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting AKAP7 exon(s) critical for AKAP 7 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 AKAP7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by AKAP 7 CRISPR/Cas9 KO Plasmid (h) and AKAP 7 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the AKAP7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by AKAP 7 HDR Plasmid (h) and AKAP 7 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by AKAP7 homology arms to support homology-directed repair at defined AKAP7 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.