FNIP2 CRISPR/Cas9 KO Plasmid (h): sc-409140
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FNIP2 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 FNIP2 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 | |
FNIP2 CRISPR/Cas9 KO Plasmid (h) | sc-409140 | 20 µg | $397.00 |
Overview
FNIP2 (folliculin interacting protein 2) is a cytoplasmic binding partner of the tumor suppressor FLCN and functions in nutrient-sensing and energy homeostasis signaling. It contributes to regulation of the AMPK–mTOR axis and participates in lysosome-associated processes that couple amino acid availability to metabolic adaptation, with downstream effects on autophagy and cellular growth control. Through its interactions with FLCN and related complexes, FNIP2 influences mitochondrial function and stress responses in metabolically active tissues. Dysregulation of FLCN–FNIP signaling has been linked to pathways implicated in inherited tumor predisposition and broader metabolic disease mechanisms, supporting its relevance in studies of cell growth and homeostasis.
FNIP2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FNIP2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FNIP2 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 FNIP2 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 FNIP2 protein expression.
This CRISPR knockout system enables efficient generation of FNIP2-deficient cell models for investigation of FNIP2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting FNIP2 exon(s) critical for FNIP2 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 FNIP2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by FNIP2 CRISPR/Cas9 KO Plasmid (h) and FNIP2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FNIP2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by FNIP2 HDR Plasmid (h) and FNIP2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FNIP2 homology arms to support homology-directed repair at defined FNIP2 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.