SMEK1 CRISPR/Cas9 KO Plasmid (h): sc-412572
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SMEK1 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 SMEK1 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 | |
SMEK1 CRISPR/Cas9 KO Plasmid (h) | sc-412572 | 20 µg | $397.00 |
Overview
PPP4R3A encodes SMEK1, a regulatory subunit of protein phosphatase 4 (PP4) that directs phosphatase activity toward specific substrates to modulate phosphorylation-dependent signaling. SMEK1 has been implicated in control of cell-cycle progression, DNA damage responses, and chromatin-associated processes through PP4-mediated dephosphorylation events that shape checkpoint signaling and nuclear protein dynamics. By influencing kinase–phosphatase balance, SMEK1 can affect pathways linked to genome stability, proliferation, and stress signaling. Dysregulation of PP4 regulatory networks, including PPP4R3A-associated functions, is relevant to studies of oncogenic signaling, replication stress, and other disorders where aberrant phosphorylation and impaired DNA repair contribute to pathology.
SMEK1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PPP4R3A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PPP4R3A 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 PPP4R3A 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 SMEK1 protein expression.
This CRISPR knockout system enables efficient generation of PPP4R3A-deficient cell models for investigation of SMEK1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting PPP4R3A exon(s) critical for SMEK1 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 PPP4R3A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SMEK1 CRISPR/Cas9 KO Plasmid (h) and SMEK1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PPP4R3A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SMEK1 HDR Plasmid (h) and SMEK1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PPP4R3A homology arms to support homology-directed repair at defined PPP4R3A 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.