Inhibin β-B CRISPR/Cas9 KO Plasmid (m): sc-421131
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Inhibin β-B 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 Inhibin β-B 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: Inhibin β-B Antibody (H-8): sc-376971
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Inhibin β-B CRISPR/Cas9 KO Plasmid (m) | sc-421131 | 20 µg | $397.00 |
Overview
Inhbb encodes inhibin beta-B, a TGF-β superfamily subunit that forms activin B homodimers or activin AB heterodimers with INHBA, modulating SMAD2/3-dependent transcription. Activin signaling regulates gonadal development, folliculogenesis, Sertoli and granulosa cell function, and broader control of cell proliferation, differentiation, and extracellular matrix remodeling. In mouse, altered Inhbb activity has been linked to reproductive phenotypes and endocrine dysregulation, and its pathway intersects with inflammatory and fibrotic programs through context-dependent control of cytokine expression and tissue remodeling. These properties make Inhbb a useful node for studying TGF-β/activin pathway wiring in developmental biology and disease-relevant cellular states.
Inhibin β-B CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Inhbb gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Inhbb 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 Inhbb 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 Inhibin β-B protein expression.
This CRISPR knockout system enables efficient generation of Inhbb-deficient cell models for investigation of Inhibin β-B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Inhbb exon(s) critical for Inhibin β-B 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 Inhbb genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Inhibin β-B CRISPR/Cas9 KO Plasmid (m) and Inhibin β-B CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Inhbb locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Inhibin β-B HDR Plasmid (m) and Inhibin β-B HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Inhbb homology arms to support homology-directed repair at defined Inhbb 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.