ADM CRISPR/Cas9 KO Plasmid (m): sc-419009
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADM 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 ADM 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 | |
ADM CRISPR/Cas9 KO Plasmid (m) | sc-419009 | 20 µg | $397.00 |
Overview
Adrenomedullin (ADM) is a secreted vasoactive peptide encoded by the mouse Adm gene that signals primarily through the calcitonin receptor-like receptor complex with RAMP2 or RAMP3, driving cAMP/PKA-dependent responses. It contributes to vascular tone regulation, endothelial barrier function, angiogenesis, and fluid–electrolyte homeostasis, and can modulate inflammatory signaling in endothelial and immune cells. ADM activity intersects with hypoxia-responsive programs and stress-adaptive pathways that influence tissue perfusion and remodeling. Dysregulated ADM expression or signaling has been associated with cardiometabolic and inflammatory disease biology, including hypertension-related vascular dysfunction and altered microvascular responses.
ADM CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Adm gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adm 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 Adm 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 ADM protein expression.
This CRISPR knockout system enables efficient generation of Adm-deficient cell models for investigation of ADM signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adm exon(s) critical for ADM 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 Adm genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ADM CRISPR/Cas9 KO Plasmid (m) and ADM CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adm locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ADM HDR Plasmid (m) and ADM HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adm homology arms to support homology-directed repair at defined Adm 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.