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.
RelB CRISPR/Cas9 KO Plasmid (m): sc-422643
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RelB 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 RelB 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: RelB Antibody (D-4): sc-48366
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RelB CRISPR/Cas9 KO Plasmid (m) | sc-422643 | 20 µg | $397.00 |
Overview
Relb encodes RelB, a member of the NF-κB/Rel family that functions predominantly in the noncanonical NF-κB pathway. RelB commonly heterodimerizes with p52 (NFKB2) to regulate transcriptional programs controlling dendritic cell maturation, lymphoid organogenesis, B cell survival, and inflammatory signaling downstream of receptors such as BAFFR, CD40, and LTβR. In mouse systems, RelB activity links innate and adaptive immune crosstalk by shaping cytokine and chemokine expression and influencing antigen presentation. Dysregulation of RelB-dependent signaling is associated with aberrant immune activation and impaired immune development, making Relb a useful target for mechanistic studies of inflammatory networks and immune cell differentiation.
RelB CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Relb gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Relb 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 Relb 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 RelB protein expression.
This CRISPR knockout system enables efficient generation of Relb-deficient cell models for investigation of RelB signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Relb exon(s) critical for RelB 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 Relb genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by RelB CRISPR/Cas9 KO Plasmid (m) and RelB CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Relb locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by RelB HDR Plasmid (m) and RelB HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Relb homology arms to support homology-directed repair at defined Relb 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.