PKC beta CRISPR/Cas9 KO Plasmid (m): sc-422259
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PKC beta 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 PKC beta 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: PKC beta 1 Antibody (E-3): sc-8049
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PKC beta CRISPR/Cas9 KO Plasmid (m) | sc-422259 | 20 µg | $397.00 |
Overview
Prkcb encodes protein kinase C beta (PKCβ), a diacylglycerol- and Ca2+-responsive serine/threonine kinase that couples receptor-dependent phospholipase C signaling to phosphorylation programs controlling proliferation, apoptosis, and differentiation. In mouse immune and hematopoietic cells, PKCβ is a key effector downstream of B cell receptor signaling, shaping NF-κB and MAPK pathway activation, cytoskeletal remodeling, and vesicular trafficking. PKCβ also regulates endothelial and smooth muscle responses through modulation of adhesion, barrier function, and oxidative stress pathways. Altered PKCβ activity has been linked to dysregulated immune signaling and inflammatory processes, supporting its relevance in mechanistic studies of cardiometabolic and vascular phenotypes.
PKC beta CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Prkcb gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Prkcb 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 Prkcb 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 PKC beta protein expression.
This CRISPR knockout system enables efficient generation of Prkcb-deficient cell models for investigation of PKC beta signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Prkcb exon(s) critical for PKC beta 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 Prkcb genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by PKC beta CRISPR/Cas9 KO Plasmid (m) and PKC beta CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Prkcb locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by PKC beta HDR Plasmid (m) and PKC beta HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Prkcb homology arms to support homology-directed repair at defined Prkcb 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.