TorsinB CRISPR/Cas9 KO Plasmid (h): sc-407379
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TorsinB 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 TorsinB 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 | |
TorsinB CRISPR/Cas9 KO Plasmid (h) | sc-407379 | 20 µg | $397.00 |
Overview
TOR1B encodes TorsinB, an AAA+ ATPase localized to the endoplasmic reticulum and perinuclear space that contributes to protein quality control and maintenance of nuclear envelope architecture. TorsinB participates in processes linked to ER homeostasis, membrane remodeling, and regulation of nuclear pore complex biogenesis, often in functional overlap with other torsin family members. Disruption of torsin-mediated pathways can perturb nucleo-cytoskeletal coupling and cellular stress responses, making TOR1B relevant to studies of neuronal function and movement disorder biology. As a human gene with roles at the ER–nuclear envelope interface, TOR1B is frequently investigated in models examining proteostasis, mechanotransduction, and organelle integrity.
TorsinB CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TOR1B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TOR1B 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 TOR1B 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 TorsinB protein expression.
This CRISPR knockout system enables efficient generation of TOR1B-deficient cell models for investigation of TorsinB signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TOR1B exon(s) critical for TorsinB 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 TOR1B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TorsinB CRISPR/Cas9 KO Plasmid (h) and TorsinB CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TOR1B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TorsinB HDR Plasmid (h) and TorsinB HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TOR1B homology arms to support homology-directed repair at defined TOR1B 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.