Troponin C slow skeletal CRISPR/Cas9 KO Plasmid (m): sc-423431
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Troponin C slow skeletal 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 Troponin C slow skeletal 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Troponin C slow skeletal CRISPR/Cas9 KO Plasmid (m) | sc-423431 | 20 µg | $397.00 |
Overview
Tnnc1 encodes troponin C slow skeletal, a Ca2+-binding regulatory subunit of the troponin complex that couples cytosolic calcium transients to actin–myosin cross-bridge cycling in striated muscle. By undergoing Ca2+-dependent conformational changes, TNNC1 modulates tropomyosin positioning on thin filaments and tunes contraction kinetics, relaxation, and energetic efficiency in slow-twitch fibers and the heart. This calcium-sensing function integrates with excitation–contraction coupling and sarcomere organization pathways, linking intracellular Ca2+ handling to myofilament responsiveness. Dysregulation of TNNC1 and thin-filament Ca2+ sensitivity is implicated in inherited cardiomyopathies and contractile dysfunction, supporting its use in studies of sarcomeric biology and muscle disease mechanisms.
Troponin C slow skeletal CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tnnc1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tnnc1 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 Tnnc1 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 Troponin C slow skeletal protein expression.
This CRISPR knockout system enables efficient generation of Tnnc1-deficient cell models for investigation of Troponin C slow skeletal signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tnnc1 exon(s) critical for Troponin C slow skeletal 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 Tnnc1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Troponin C slow skeletal CRISPR/Cas9 KO Plasmid (m) and Troponin C slow skeletal CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tnnc1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Troponin C slow skeletal HDR Plasmid (m) and Troponin C slow skeletal HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tnnc1 homology arms to support homology-directed repair at defined Tnnc1 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.