D53 CRISPR/Cas9 KO Plasmid (m): sc-423478
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- D53 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 D53 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 | |
D53 CRISPR/Cas9 KO Plasmid (m) | sc-423478 | 20 µg | $397.00 |
Overview
Tpd52l1 encodes D53, a cytosolic protein in the tumor protein D52-like family that has been linked to regulation of membrane trafficking, vesicle dynamics, and cytoskeletal organization. In mouse cells, D53 is associated with processes that coordinate secretion, cell polarity, and proliferation, and it has been reported to interface with signaling programs that shape epithelial and stromal cell behavior. Altered expression of D52-family members has been observed in contexts of oncogenic transformation and abnormal growth control, making Tpd52l1 a useful target for dissecting mechanisms of cell-cycle progression, migration, and stress-adaptive remodeling. Genetic perturbation of Tpd52l1 supports studies of pathway connectivity between trafficking machinery, mitogenic signaling, and phenotypes relevant to tumor biology and tissue homeostasis.
D53 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tpd52l1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tpd52l1 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 Tpd52l1 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 D53 protein expression.
This CRISPR knockout system enables efficient generation of Tpd52l1-deficient cell models for investigation of D53 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tpd52l1 exon(s) critical for D53 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 Tpd52l1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by D53 CRISPR/Cas9 KO Plasmid (m) and D53 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tpd52l1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by D53 HDR Plasmid (m) and D53 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tpd52l1 homology arms to support homology-directed repair at defined Tpd52l1 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.