TP53INP2 CRISPR/Cas9 KO Plasmid (m): sc-427155
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TP53INP2 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 TP53INP2 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 | |
TP53INP2 CRISPR/Cas9 KO Plasmid (m) | sc-427155 | 20 µg | $397.00 |
Overview
Trp53inp2 encodes TP53INP2, a stress-inducible nuclear and cytoplasmic protein implicated in regulation of autophagy and transcriptional programs linked to cellular homeostasis. TP53INP2 has been reported to participate in autophagosome formation and trafficking through interactions with autophagy machinery, supporting nutrient-sensing and organelle quality control pathways. In mouse models and cell systems, TP53INP2 activity is commonly examined in the context of metabolic adaptation, cell survival decisions, and responses to oxidative or genotoxic stress. Dysregulation of TP53INP2-associated autophagy and stress signaling is relevant to studies of tumor biology, inflammatory states, and neurodegenerative processes where altered proteostasis is a key feature.
TP53INP2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trp53inp2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trp53inp2 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 Trp53inp2 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 TP53INP2 protein expression.
This CRISPR knockout system enables efficient generation of Trp53inp2-deficient cell models for investigation of TP53INP2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trp53inp2 exon(s) critical for TP53INP2 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 Trp53inp2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TP53INP2 CRISPR/Cas9 KO Plasmid (m) and TP53INP2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trp53inp2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TP53INP2 HDR Plasmid (m) and TP53INP2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trp53inp2 homology arms to support homology-directed repair at defined Trp53inp2 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.