Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ADAM4 CRISPR/Cas9 KO Plasmid (m): sc-418990
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADAM4 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 ADAM4 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: ADAM4 Antibody (D-4): sc-390853
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADAM4 CRISPR/Cas9 KO Plasmid (m) | sc-418990 | 20 µg | $397.00 |
Overview
Adam4 encodes ADAM4, a member of the ADAM (a disintegrin and metalloprotease) family implicated in membrane-proximal proteolysis and cell–cell or cell–matrix interactions. ADAM proteins can modulate extracellular domain shedding of surface receptors and adhesion molecules, influencing signaling dynamics, inflammatory cues, and tissue remodeling. In mouse systems, ADAM4 is studied in the context of protease-dependent regulation of developmental and reproductive processes as well as microenvironmental regulation of cell behavior. Dysregulation of ADAM-family proteolysis is broadly relevant to pathological remodeling and aberrant signaling, providing a mechanistic entry point for dissecting protease-driven phenotypes.
ADAM4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Adam4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Adam4 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 Adam4 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 ADAM4 protein expression.
This CRISPR knockout system enables efficient generation of Adam4-deficient cell models for investigation of ADAM4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Adam4 exon(s) critical for ADAM4 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 Adam4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ADAM4 CRISPR/Cas9 KO Plasmid (m) and ADAM4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Adam4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ADAM4 HDR Plasmid (m) and ADAM4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Adam4 homology arms to support homology-directed repair at defined Adam4 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.