ADAM5 CRISPR/Cas9 KO Plasmid (m): sc-418991
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADAM5 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 ADAM5 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: ADAM5 Antibody (C-6): sc-390150
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADAM5 CRISPR/Cas9 KO Plasmid (m) | sc-418991 | 20 µg | $397.00 |
Overview
Adam5 encodes ADAM5, a member of the ADAM (a disintegrin and metalloproteinase) family implicated in membrane-associated proteolysis and cell–cell or cell–matrix interactions. ADAM proteins can influence ectodomain shedding of surface proteins, thereby shaping signaling dynamics, adhesion, and tissue remodeling processes. In mouse systems, ADAM5 is studied in the context of protease-dependent regulation of developmental and reproductive biology, with potential links to pathways governing cell communication and extracellular environment sensing. Dysregulation of related ADAM family activities is associated with inflammatory signaling and cancer-relevant phenotypes, making Adam5 a useful target for mechanistic studies of proteolysis-driven signaling networks.
ADAM5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Adam5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adam5 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 Adam5 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 ADAM5 protein expression.
This CRISPR knockout system enables efficient generation of Adam5-deficient cell models for investigation of ADAM5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adam5 exon(s) critical for ADAM5 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 Adam5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ADAM5 CRISPR/Cas9 KO Plasmid (m) and ADAM5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adam5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ADAM5 HDR Plasmid (m) and ADAM5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adam5 homology arms to support homology-directed repair at defined Adam5 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.