Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CLN2 CRISPR/Cas9 KO Plasmid (h): sc-405204
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CLN2 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 CLN2 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: CLN2 Antibody (G-3): sc-393961
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CLN2 CRISPR/Cas9 KO Plasmid (h) | sc-405204 | 20 µg | $397.00 |
Overview
TPP1 encodes tripeptidyl peptidase 1 (CLN2), a lysosomal serine protease that removes tripeptides from the N-termini of polypeptides during intralysosomal protein turnover. CLN2 activity supports lysosome-dependent catabolic processes that intersect with autophagy–lysosome flux, endolysosomal trafficking, and proteostasis maintenance in metabolically active cell types. Loss of TPP1 function disrupts lysosomal proteolysis and contributes to neuronal vulnerability, with pathogenic variants linked to CLN2-related neuronal ceroid lipofuscinosis and broader lysosomal storage pathology. Consequently, TPP1/CLN2 is widely studied in models of lysosomal function, stress responses, and mechanisms coupling impaired degradation to cellular dysfunction.
CLN2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TPP1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TPP1 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 TPP1 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 CLN2 protein expression.
This CRISPR knockout system enables efficient generation of TPP1-deficient cell models for investigation of CLN2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TPP1 exon(s) critical for CLN2 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 TPP1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CLN2 CRISPR/Cas9 KO Plasmid (h) and CLN2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TPP1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CLN2 HDR Plasmid (h) and CLN2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TPP1 homology arms to support homology-directed repair at defined TPP1 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.