Inhibin β-C CRISPR/Cas9 KO Plasmid (m): sc-421132
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Inhibin β-C 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-C 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 | |
Inhibin β-C CRISPR/Cas9 KO Plasmid (m) | sc-421132 | 20 µg | $397.00 |
Overview
Inhbc encodes the mouse Inhibin beta-C subunit, a member of the TGF-β superfamily that can contribute to the formation of activin and inhibin ligands, thereby influencing SMAD-dependent signaling. Through modulation of TGF-β/activin pathway activity, Inhibin β-C is implicated in regulation of cellular differentiation programs, tissue homeostasis, and context-dependent control of proliferation. Altered balance of activin/inhibin signaling is associated with dysregulated inflammatory and fibrotic responses and has been linked to changes in reproductive and endocrine-related processes in multiple model systems. In mouse research, Inhbc provides a tractable node for dissecting ligand availability and downstream transcriptional responses within TGF-β superfamily networks.
Inhibin β-C CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Inhbc gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Inhbc 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 Inhbc 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-C protein expression.
This CRISPR knockout system enables efficient generation of Inhbc-deficient cell models for investigation of Inhibin β-C signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Inhbc exon(s) critical for Inhibin β-C 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 Inhbc genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Inhibin β-C CRISPR/Cas9 KO Plasmid (m) and Inhibin β-C CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Inhbc locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Inhibin β-C HDR Plasmid (m) and Inhibin β-C HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Inhbc homology arms to support homology-directed repair at defined Inhbc 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.