RECK CRISPR/Cas9 KO Plasmid (h): sc-402440
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RECK 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 RECK 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: RECK Antibody (G-4): sc-373929
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RECK CRISPR/Cas9 KO Plasmid (h) | sc-402440 | 20 µg | $397.00 |
Overview
RECK (reversion-inducing cysteine-rich protein with Kazal motifs) is a membrane-anchored regulator of extracellular matrix remodeling that suppresses the activity of multiple matrix metalloproteinases, including MMP2, MMP9, and MT1-MMP. By constraining pericellular proteolysis, RECK influences cell–matrix adhesion, migration, and invasion, and intersects with pathways governing angiogenesis and tissue morphogenesis. RECK expression is frequently reduced in diverse tumor contexts and is associated with altered invasive behavior and metastatic potential, making it a key node in studies of microenvironment-driven disease phenotypes. In addition, RECK-dependent control of protease activity links it to inflammatory remodeling and fibrosis-related processes where ECM turnover is dysregulated.
RECK CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the RECK gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the RECK 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 RECK 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 RECK protein expression.
This CRISPR knockout system enables efficient generation of RECK-deficient cell models for investigation of RECK signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting RECK exon(s) critical for RECK 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 RECK genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RECK CRISPR/Cas9 KO Plasmid (h) and RECK CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the RECK locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RECK HDR Plasmid (h) and RECK HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by RECK homology arms to support homology-directed repair at defined RECK 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.