Tβ-4 CRISPR/Cas9 KO Plasmid (m): sc-422497
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tβ-4 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 Tβ-4 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: Tβ-4 Antibody (4H7): sc-293251
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tβ-4 CRISPR/Cas9 KO Plasmid (m) | sc-422497 | 20 µg | $397.00 |
Overview
Tmsb4x encodes thymosin β-4 (Tβ-4), a highly conserved actin-sequestering peptide that regulates G-actin availability and supports dynamic remodeling of the cytoskeleton. In mouse cells, Tβ-4 influences processes including cell migration, adhesion, wound-associated motility, and cytoskeletal organization through modulation of actin polymerization and downstream signaling linked to focal adhesion and Rho-family GTPase pathways. By shaping actin-dependent trafficking and cellular stress responses, Tmsb4x has been studied in contexts such as inflammation, tissue remodeling, angiogenic programs, and fibrotic progression. Dysregulated actin dynamics associated with altered Tβ-4 activity can impact proliferative and migratory phenotypes relevant to cancer biology and immune cell function.
Tβ-4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tmsb4x gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tmsb4x 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 Tmsb4x 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 Tβ-4 protein expression.
This CRISPR knockout system enables efficient generation of Tmsb4x-deficient cell models for investigation of Tβ-4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tmsb4x exon(s) critical for Tβ-4 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 Tmsb4x genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Tβ-4 CRISPR/Cas9 KO Plasmid (m) and Tβ-4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tmsb4x locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Tβ-4 HDR Plasmid (m) and Tβ-4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tmsb4x homology arms to support homology-directed repair at defined Tmsb4x 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.