TBL2 CRISPR/Cas9 KO Plasmid (h): sc-407010
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TBL2 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 TBL2 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 | |
TBL2 CRISPR/Cas9 KO Plasmid (h) | sc-407010 | 20 µg | $397.00 |
Overview
TBL2 (transducin beta-like 2) is an endoplasmic reticulum–associated protein implicated in membrane-proximal signaling and proteostasis, with reported roles in regulating cellular stress responses and translational control. By linking ER homeostasis to signaling networks, TBL2 is studied in contexts where unfolded protein handling, lipid and membrane biology, and adaptive stress pathways influence cell fate decisions. Altered regulation of ER stress and related metabolic signaling has been associated with inflammatory and metabolic phenotypes, making TBL2 a useful target for mechanistic studies in these processes. In human cell models, perturbing TBL2 supports investigation of how ER-linked signaling nodes shape pathway output under nutrient, oxidative, or proteotoxic stress.
TBL2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TBL2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TBL2 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 TBL2 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 TBL2 protein expression.
This CRISPR knockout system enables efficient generation of TBL2-deficient cell models for investigation of TBL2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TBL2 exon(s) critical for TBL2 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 TBL2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TBL2 CRISPR/Cas9 KO Plasmid (h) and TBL2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TBL2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TBL2 HDR Plasmid (h) and TBL2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TBL2 homology arms to support homology-directed repair at defined TBL2 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.