NALP10 CRISPR/Cas9 KO Plasmid (h): sc-406528
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NALP10 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 NALP10 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 | |
NALP10 CRISPR/Cas9 KO Plasmid (h) | sc-406528 | 20 µg | $397.00 |
Overview
NLRP10 (NALP10) is a member of the NOD-like receptor family implicated in regulating innate immune signaling and inflammatory homeostasis. Unlike canonical inflammasome-forming NLRs, NLRP10 has been linked to modulation of NF-κB–dependent transcription, cytokine responses, and control of inflammasome-associated outputs in a context-dependent manner. It contributes to antigen-presenting cell function, including effects on dendritic cell migration and T cell priming, positioning NLRP10 within pathways that shape immune activation and tolerance. Altered NLRP10 activity has been associated with immune dysregulation and inflammatory phenotypes, supporting its use as a target for mechanistic studies in immunology and host-response models.
NALP10 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the NLRP10 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the NLRP10 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 NLRP10 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 NALP10 protein expression.
This CRISPR knockout system enables efficient generation of NLRP10-deficient cell models for investigation of NALP10 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting NLRP10 exon(s) critical for NALP10 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 NLRP10 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NALP10 CRISPR/Cas9 KO Plasmid (h) and NALP10 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the NLRP10 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NALP10 HDR Plasmid (h) and NALP10 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by NLRP10 homology arms to support homology-directed repair at defined NLRP10 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.