Gα t2 CRISPR/Cas9 KO Plasmid (h): sc-401528
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Gα t2 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 Gα t2 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 | |
Gα t2 CRISPR/Cas9 KO Plasmid (h) | sc-401528 | 20 µg | $397.00 |
Overview
GNAT2 encodes the alpha subunit of transducin (Gαt2), a heterotrimeric G protein that couples activated opsins to downstream effectors in phototransduction. Upon GPCR stimulation, Gαt2 exchanges GDP for GTP, dissociates from Gβγ, and modulates cyclic nucleotide signaling to shape cellular excitability and stimulus-dependent responses. Although best characterized in retinal signaling contexts, GNAT2 provides a tractable entry point for studying GPCR–G protein coupling, GTPase cycle regulation, and signal termination mechanisms that interface with cGMP metabolism and ion channel control. Genetic perturbation of GNAT2 has been linked to inherited visual dysfunction phenotypes, supporting its relevance for modeling sensory signaling defects and pathway compensation.
Gα t2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the GNAT2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the GNAT2 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 GNAT2 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 Gα t2 protein expression.
This CRISPR knockout system enables efficient generation of GNAT2-deficient cell models for investigation of Gα t2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting GNAT2 exon(s) critical for Gα t2 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 GNAT2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Gα t2 CRISPR/Cas9 KO Plasmid (h) and Gα t2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the GNAT2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Gα t2 HDR Plasmid (h) and Gα t2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by GNAT2 homology arms to support homology-directed repair at defined GNAT2 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.