Tropomyosin γ CRISPR/Cas9 KO Plasmid (h): sc-401764
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Tropomyosin γ 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 Tropomyosin γ 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 γ Antibody (164J2U): sc-517613
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Tropomyosin γ CRISPR/Cas9 KO Plasmid (h) | sc-401764 | 20 µg | $397.00 |
Overview
TPM3 encodes human tropomyosin gamma, an actin-binding coiled-coil protein that stabilizes filamentous actin and regulates access of myosins and actin-associated factors to the cytoskeleton. By modulating actin filament dynamics, TPM3 contributes to cytoskeletal remodeling processes including cell shape control, adhesion, migration, and contractile function. Tropomyosin isoforms help specify distinct actin filament populations that interface with signaling pathways governing mechanotransduction and stress fiber organization. Altered TPM3 expression or rearrangements involving TPM3 are linked to dysregulated cytoskeletal architecture and have been reported in contexts such as oncogenic fusion events and neuromuscular phenotypes, making it relevant for investigating cytoskeleton-driven disease mechanisms.
Tropomyosin γ CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TPM3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TPM3 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 TPM3 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 γ protein expression.
This CRISPR knockout system enables efficient generation of TPM3-deficient cell models for investigation of Tropomyosin γ signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TPM3 exon(s) critical for Tropomyosin γ 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 TPM3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Tropomyosin γ CRISPR/Cas9 KO Plasmid (h) and Tropomyosin γ CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TPM3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Tropomyosin γ HDR Plasmid (h) and Tropomyosin γ HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TPM3 homology arms to support homology-directed repair at defined TPM3 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.