TTC7A CRISPR/Cas9 KO Plasmid (h): sc-412780
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TTC7A 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 TTC7A 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 | |
TTC7A CRISPR/Cas9 KO Plasmid (h) | sc-412780 | 20 µg | $397.00 |
Overview
TTC7A encodes a tetratricopeptide repeat–containing protein implicated in organizing multiprotein assemblies that support epithelial polarity and cytoskeletal homeostasis. Studies link TTC7A to phosphoinositide-related signaling and membrane trafficking processes that influence cell adhesion, actin dynamics, and intestinal epithelial integrity. Loss-of-function variants have been associated with severe early-onset intestinal and immune phenotypes, making TTC7A a useful entry point for dissecting mechanisms of epithelial barrier dysfunction and immune dysregulation. In human cell models, perturbing TTC7A can help interrogate pathway cross-talk between membrane organization, stress responses, and lineage-specific differentiation programs.
TTC7A CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TTC7A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TTC7A 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 TTC7A 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 TTC7A protein expression.
This CRISPR knockout system enables efficient generation of TTC7A-deficient cell models for investigation of TTC7A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TTC7A exon(s) critical for TTC7A 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 TTC7A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TTC7A CRISPR/Cas9 KO Plasmid (h) and TTC7A CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TTC7A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TTC7A HDR Plasmid (h) and TTC7A HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TTC7A homology arms to support homology-directed repair at defined TTC7A 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.