ACTR-IB CRISPR/Cas9 KO Plasmid (m): sc-418975
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ACTR-IB 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 ACTR-IB 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: ACTR-IB Antibody (ALEX66): sc-73677
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACTR-IB CRISPR/Cas9 KO Plasmid (m) | sc-418975 | 20 µg | $397.00 |
Overview
Acvr1b encodes activin A receptor type 1B (ACTR-IB/ALK4), a serine/threonine kinase receptor in the TGF-β superfamily that transduces signals from activins and related ligands. Upon ligand engagement and receptor complex formation, ACTR-IB phosphorylates SMAD2/3 to regulate transcriptional programs controlling cell fate decisions, proliferation, differentiation, and tissue remodeling. In mouse systems, Acvr1b-dependent signaling integrates with MAPK and other context-specific pathways to shape developmental and homeostatic responses. Dysregulation of activin/SMAD signaling is commonly used to model mechanisms relevant to fibrosis, inflammation, metabolic regulation, and oncogenic phenotypes in experimental settings.
ACTR-IB CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Acvr1b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Acvr1b 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 Acvr1b 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 ACTR-IB protein expression.
This CRISPR knockout system enables efficient generation of Acvr1b-deficient cell models for investigation of ACTR-IB signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Acvr1b exon(s) critical for ACTR-IB 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 Acvr1b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by ACTR-IB CRISPR/Cas9 KO Plasmid (m) and ACTR-IB CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Acvr1b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by ACTR-IB HDR Plasmid (m) and ACTR-IB HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Acvr1b homology arms to support homology-directed repair at defined Acvr1b 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.