BCMA CRISPR/Cas9 KO Plasmid (m): sc-423440
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BCMA 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 BCMA 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: BCMA Antibody (D-6): sc-390147
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BCMA CRISPR/Cas9 KO Plasmid (m) | sc-423440 | 20 µg | $397.00 |
Overview
Tnfrsf17 encodes B cell maturation antigen (BCMA), a TNF receptor superfamily member predominantly expressed on plasma cells and late-stage B cells. BCMA binds APRIL and BAFF to activate canonical and non-canonical NF-κB, MAPK, and PI3K/AKT signaling, promoting plasma cell survival, immunoglobulin secretion, and maintenance of humoral immunity. In mouse models, BCMA-dependent signaling shapes B cell differentiation and antibody responses, linking Tnfrsf17 to immune homeostasis and inflammation-associated tissue pathology. Dysregulated BCMA signaling and plasma cell expansion are widely used as molecular readouts in studies of autoimmune-like phenotypes and B cell lineage dysregulation.
BCMA CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tnfrsf17 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tnfrsf17 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 Tnfrsf17 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 BCMA protein expression.
This CRISPR knockout system enables efficient generation of Tnfrsf17-deficient cell models for investigation of BCMA signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tnfrsf17 exon(s) critical for BCMA 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 Tnfrsf17 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BCMA CRISPR/Cas9 KO Plasmid (m) and BCMA CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tnfrsf17 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BCMA HDR Plasmid (m) and BCMA HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tnfrsf17 homology arms to support homology-directed repair at defined Tnfrsf17 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.