TBX5 CRISPR/Cas9 KO Plasmid (m): sc-423282
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TBX5 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 TBX5 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: TBX5 Antibody (A-4): sc-376952
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TBX5 CRISPR/Cas9 KO Plasmid (m) | sc-423282 | 20 µg | $397.00 |
Overview
Tbx5 encodes the T-box transcription factor TBX5, a sequence-specific DNA-binding regulator that coordinates developmental gene programs controlling forelimb patterning and cardiac morphogenesis in mouse. TBX5 integrates with core transcriptional networks involving NKX2-5, GATA4, and MEF2 family factors to modulate enhancer activity and lineage specification in mesoderm-derived tissues. Its activity influences pathways governing chamber formation, conduction system development, and cardiomyocyte differentiation, and perturbation of Tbx5 dosage is linked to congenital heart and limb malformation phenotypes. As a developmental regulator with context-dependent targets, TBX5 is widely used to study transcriptional control of organogenesis and cell fate decisions.
TBX5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tbx5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tbx5 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 Tbx5 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 TBX5 protein expression.
This CRISPR knockout system enables efficient generation of Tbx5-deficient cell models for investigation of TBX5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tbx5 exon(s) critical for TBX5 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 Tbx5 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TBX5 CRISPR/Cas9 KO Plasmid (m) and TBX5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tbx5 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TBX5 HDR Plasmid (m) and TBX5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tbx5 homology arms to support homology-directed repair at defined Tbx5 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.