ADAMTS-7 CRISPR/Cas9 KO Plasmid (h): sc-403381
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADAMTS-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 ADAMTS-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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADAMTS-7 CRISPR/Cas9 KO Plasmid (h) | sc-403381 | 20 µg | $397.00 |
Overview
ADAMTS7 encodes ADAMTS-7, a secreted metalloprotease of the ADAMTS family that remodels the extracellular matrix by proteolytic processing of matrix components and associated proteins. In human tissues, ADAMTS-7 activity influences cell–matrix interactions, vascular smooth muscle cell behavior, and matrix turnover pathways that shape tissue architecture and inflammatory remodeling. Dysregulated ADAMTS7 expression or activity has been linked to vascular pathology and atherosclerosis-related processes, and altered extracellular matrix dynamics may also intersect with fibrotic and degenerative tissue responses. These features make ADAMTS-7 a useful target for studying extracellular proteostasis, matrix signaling, and disease-relevant remodeling phenotypes in cell-based and mechanistic models.
ADAMTS-7 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ADAMTS7 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ADAMTS7 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 ADAMTS7 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 ADAMTS-7 protein expression.
This CRISPR knockout system enables efficient generation of ADAMTS7-deficient cell models for investigation of ADAMTS-7 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting ADAMTS7 exon(s) critical for ADAMTS-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 ADAMTS7 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ADAMTS-7 CRISPR/Cas9 KO Plasmid (h) and ADAMTS-7 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ADAMTS7 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ADAMTS-7 HDR Plasmid (h) and ADAMTS-7 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ADAMTS7 homology arms to support homology-directed repair at defined ADAMTS7 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.