OLFM3 CRISPR/Cas9 KO Plasmid (h): sc-406216
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OLFM3 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 OLFM3 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: OLFM3 Antibody (M-N16): sc-100795
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OLFM3 CRISPR/Cas9 KO Plasmid (h) | sc-406216 | 20 µg | $397.00 |
Overview
OLFM3 (olfactomedin 3) encodes a secreted glycoprotein of the olfactomedin domain family that localizes to the extracellular space and participates in cell–cell and cell–matrix interactions. OLFM3 has been linked to modulation of immune and inflammatory signaling in tissue microenvironments and is associated with processes such as extracellular matrix organization, cellular adhesion, and regulation of myeloid cell behavior. Altered OLFM3 expression has been reported across multiple disease contexts, including cancer biology and inflammatory conditions, where it may correlate with changes in tumor–immune crosstalk and stromal remodeling. These features make OLFM3 a useful target for mechanistic studies of microenvironmental signaling and extracellular regulatory networks.
OLFM3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the OLFM3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the OLFM3 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 OLFM3 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 OLFM3 protein expression.
This CRISPR knockout system enables efficient generation of OLFM3-deficient cell models for investigation of OLFM3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting OLFM3 exon(s) critical for OLFM3 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 OLFM3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by OLFM3 CRISPR/Cas9 KO Plasmid (h) and OLFM3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the OLFM3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by OLFM3 HDR Plasmid (h) and OLFM3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by OLFM3 homology arms to support homology-directed repair at defined OLFM3 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.