TIMP-4 CRISPR/Cas9 KO Plasmid (h): sc-402560
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TIMP-4 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 TIMP-4 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 | |
TIMP-4 CRISPR/Cas9 KO Plasmid (h) | sc-402560 | 20 µg | $397.00 |
Overview
TIMP4 encodes tissue inhibitor of metalloproteinases-4 (TIMP-4), a secreted endogenous inhibitor that binds and restrains matrix metalloproteinases to regulate extracellular matrix (ECM) turnover. By modulating pericellular proteolysis, TIMP-4 influences cell adhesion, migration, and tissue remodeling programs that interface with ECM–integrin signaling, inflammatory cues, and growth factor availability. Altered TIMP4 expression or TIMP/MMP balance is frequently studied in contexts of fibrosis, vascular remodeling, and tumor microenvironment dynamics where ECM composition and protease activity shape cellular phenotypes. TIMP-4 also participates in controlling protease-dependent processing of bioactive molecules, making it relevant for pathway mapping in matrix biology and proteostasis.
TIMP-4 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TIMP4 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TIMP4 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 TIMP4 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 TIMP-4 protein expression.
This CRISPR knockout system enables efficient generation of TIMP4-deficient cell models for investigation of TIMP-4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TIMP4 exon(s) critical for TIMP-4 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 TIMP4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TIMP-4 CRISPR/Cas9 KO Plasmid (h) and TIMP-4 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TIMP4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TIMP-4 HDR Plasmid (h) and TIMP-4 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TIMP4 homology arms to support homology-directed repair at defined TIMP4 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.