BTG3 CRISPR/Cas9 KO Plasmid (h): sc-407253
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BTG3 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 BTG3 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 | |
BTG3 CRISPR/Cas9 KO Plasmid (h) | sc-407253 | 20 µg | $397.00 |
Overview
BTG3 (B-cell translocation gene 3) encodes an antiproliferative protein in the BTG/TOB family that helps coordinate cell-cycle control and cellular differentiation. BTG3 functions as a transcriptional coregulator and interacts with pathways governing G1/S transition, DNA damage responses, and apoptotic signaling, linking its activity to maintenance of genomic stability. Altered BTG3 expression has been reported in multiple tumor contexts and is commonly associated with dysregulated proliferation, stress-response signaling, and changes in differentiation state, making it a useful node for mechanistic studies of growth control.
BTG3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the BTG3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the BTG3 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 BTG3 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 BTG3 protein expression.
This CRISPR knockout system enables efficient generation of BTG3-deficient cell models for investigation of BTG3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting BTG3 exon(s) critical for BTG3 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 BTG3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BTG3 CRISPR/Cas9 KO Plasmid (h) and BTG3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the BTG3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BTG3 HDR Plasmid (h) and BTG3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by BTG3 homology arms to support homology-directed repair at defined BTG3 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.