Apelin CRISPR/Cas9 KO Plasmid (h): sc-401548
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Apelin 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 Apelin 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: Apelin Antibody (2A1-2D5): sc-293441
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Apelin CRISPR/Cas9 KO Plasmid (h) | sc-401548 | 20 µg | $397.00 |
Overview
APLN encodes apelin, a secreted peptide ligand for the APJ receptor (APLNR) that regulates cardiovascular homeostasis, angiogenesis, fluid balance, and metabolic signaling. Apelin–APJ engagement activates GPCR-driven pathways including PI3K/AKT, ERK/MAPK, and AMPK, shaping endothelial migration, vascular tone, and cellular energy utilization. In human tissues, apelin expression is responsive to hypoxia and inflammatory cues and is frequently studied in the context of vascular remodeling and adipose biology. Dysregulated APLN signaling has been associated with cardiometabolic phenotypes, pulmonary and systemic vascular dysfunction, and tumor microenvironment processes such as neovascularization.
Apelin CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the APLN gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the APLN 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 APLN 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 Apelin protein expression.
This CRISPR knockout system enables efficient generation of APLN-deficient cell models for investigation of Apelin signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting APLN exon(s) critical for Apelin 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 APLN genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Apelin CRISPR/Cas9 KO Plasmid (h) and Apelin CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the APLN locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Apelin HDR Plasmid (h) and Apelin HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by APLN homology arms to support homology-directed repair at defined APLN 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.