Tropomyosin α CRISPR/Cas9 KO Plasmid (m): sc-423481
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tropomyosin α 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 Tropomyosin α 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: Tropomyosin α Antibody (F-6): sc-376541
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tropomyosin α CRISPR/Cas9 KO Plasmid (m) | sc-423481 | 20 µg | $397.00 |
Overview
Mouse Tpm1 encodes tropomyosin α, an actin-binding coiled-coil protein that stabilizes filamentous actin and specifies actomyosin function by regulating myosin access to actin. Tropomyosin α contributes to cytoskeletal architecture, stress fiber formation, and contractile dynamics that shape cell adhesion, migration, and mechanotransduction. Through its role in actin filament organization, TPM1 intersects with pathways governing sarcomeric and non-muscle actin remodeling, including Rho GTPase–dependent cytoskeletal regulation. Altered tropomyosin isoform balance and TPM1-dependent actin regulation have been associated with defects in muscle function and broader cytoskeletal dysregulation relevant to cardiomyopathy and tumor cell motility models.
Tropomyosin α CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tpm1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tpm1 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 Tpm1 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 Tropomyosin α protein expression.
This CRISPR knockout system enables efficient generation of Tpm1-deficient cell models for investigation of Tropomyosin α signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tpm1 exon(s) critical for Tropomyosin α 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 Tpm1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Tropomyosin α CRISPR/Cas9 KO Plasmid (m) and Tropomyosin α CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tpm1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Tropomyosin α HDR Plasmid (m) and Tropomyosin α HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tpm1 homology arms to support homology-directed repair at defined Tpm1 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.