PISD CRISPR/Cas9 KO Plasmid (h): sc-404398
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PISD 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 PISD 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: PISD Antibody (H-2): sc-390070
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PISD CRISPR/Cas9 KO Plasmid (h) | sc-404398 | 20 µg | $397.00 |
Overview
PISD encodes phosphatidylserine decarboxylase, a mitochondrial inner-membrane enzyme that converts phosphatidylserine to phosphatidylethanolamine, supporting membrane biogenesis, cristae architecture, and organelle homeostasis. By controlling the PE pool, PISD influences lipid remodeling, mitochondrial dynamics, and processes linked to oxidative phosphorylation and apoptosis. Perturbation of PISD-dependent phospholipid metabolism has been connected to defects in mitochondrial function and broader cellular stress responses, making it relevant to studies of neuromuscular and metabolic phenotypes. Its central role in mitochondrial lipid biosynthesis also intersects with pathways that regulate autophagy and ER–mitochondria lipid trafficking.
PISD CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PISD gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PISD 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 PISD 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 PISD protein expression.
This CRISPR knockout system enables efficient generation of PISD-deficient cell models for investigation of PISD signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PISD exon(s) critical for PISD 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 PISD genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PISD CRISPR/Cas9 KO Plasmid (h) and PISD CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PISD locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PISD HDR Plasmid (h) and PISD HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PISD homology arms to support homology-directed repair at defined PISD 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.