BTG1 CRISPR/Cas9 KO Plasmid (h): sc-405339
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BTG1 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 BTG1 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: BTG1 Antibody (2095C1a): sc-81207
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BTG1 CRISPR/Cas9 KO Plasmid (h) | sc-405339 | 20 µg | $397.00 |
Overview
BTG1 (B-cell translocation gene 1) encodes an antiproliferative regulator that modulates cell-cycle progression and cellular quiescence, with prominent roles in hematopoietic differentiation and lymphoid homeostasis. BTG1 protein functions as a transcriptional coregulator and interfaces with mRNA deadenylation machinery (CCR4–NOT complex) via interactions with factors such as CAF1/CNOT7, shaping transcript stability and gene expression programs. Through these activities, BTG1 influences signaling outputs linked to stress responses and developmental checkpoints, including pathways governing proliferation, apoptosis, and differentiation. Altered BTG1 expression or genetic lesions are recurrently associated with lymphoid malignancy biology and treatment-response phenotypes, making it a useful target for mechanistic studies of tumor suppressor-like processes and transcriptional control.
BTG1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the BTG1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the BTG1 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 BTG1 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 BTG1 protein expression.
This CRISPR knockout system enables efficient generation of BTG1-deficient cell models for investigation of BTG1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting BTG1 exon(s) critical for BTG1 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 BTG1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by BTG1 CRISPR/Cas9 KO Plasmid (h) and BTG1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the BTG1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by BTG1 HDR Plasmid (h) and BTG1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by BTG1 homology arms to support homology-directed repair at defined BTG1 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.