PAFAH1B3 CRISPR/Cas9 KO Plasmid (m): sc-422104
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PAFAH1B3 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 PAFAH1B3 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: PAFAH1B3 Antibody (37-K): sc-81950
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PAFAH1B3 CRISPR/Cas9 KO Plasmid (m) | sc-422104 | 20 µg | $397.00 |
Overview
Pafah1b3 encodes the catalytic subunit PAFAH1B3, a serine-dependent phospholipase that hydrolyzes platelet-activating factor and related bioactive phospholipids. By modulating lipid second messengers, PAFAH1B3 contributes to membrane homeostasis and influences downstream inflammatory signaling, stress responses, and metabolic remodeling pathways. Altered PAFAH1B3 activity has been linked to shifts in cellular lipid composition and proliferation-associated programs, supporting its relevance in studies of cancer cell metabolism and immune regulation. In mouse models, Pafah1b3 provides a tractable entry point to interrogate phospholipid catabolism and its impact on tissue physiology and disease-associated lipid signaling.
PAFAH1B3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Pafah1b3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Pafah1b3 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 Pafah1b3 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 PAFAH1B3 protein expression.
This CRISPR knockout system enables efficient generation of Pafah1b3-deficient cell models for investigation of PAFAH1B3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Pafah1b3 exon(s) critical for PAFAH1B3 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 Pafah1b3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PAFAH1B3 CRISPR/Cas9 KO Plasmid (m) and PAFAH1B3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Pafah1b3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PAFAH1B3 HDR Plasmid (m) and PAFAH1B3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Pafah1b3 homology arms to support homology-directed repair at defined Pafah1b3 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.