T1R3 CRISPR/Cas9 KO Plasmid (h): sc-401808
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- T1R3 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 T1R3 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 | |
T1R3 CRISPR/Cas9 KO Plasmid (h) | sc-401808 | 20 µg | $397.00 |
Overview
TAS1R3 encodes the human taste receptor subunit T1R3, a class C GPCR that heterodimerizes with T1R1 or T1R2 to sense umami- and sweet-associated ligands. Upon activation, T1R3-linked signaling engages heterotrimeric G proteins and downstream PLCβ2–IP3–Ca²⁺ flux, leading to effector responses that can influence secretion and cellular excitability. Beyond gustatory tissues, TAS1R3 expression in extraoral epithelia and metabolic organs has been used to interrogate nutrient-sensing circuits that intersect with endocrine and inflammatory processes. Dysregulation of sweet/umami receptor signaling has been explored in studies of metabolic homeostasis and chemosensory defects, supporting its relevance as a molecular handle for pathway-level research.
T1R3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TAS1R3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TAS1R3 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 TAS1R3 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 T1R3 protein expression.
This CRISPR knockout system enables efficient generation of TAS1R3-deficient cell models for investigation of T1R3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting TAS1R3 exon(s) critical for T1R3 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 TAS1R3 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by T1R3 CRISPR/Cas9 KO Plasmid (h) and T1R3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TAS1R3 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by T1R3 HDR Plasmid (h) and T1R3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TAS1R3 homology arms to support homology-directed repair at defined TAS1R3 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.