TSHR CRISPR/Cas9 KO Plasmid (m): sc-423527
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TSHR CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 TSHR 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TSHR Antibody (3B12): sc-53542
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TSHR CRISPR/Cas9 KO Plasmid (m) | sc-423527 | 20 µg | $397.00 |
Overview
Tshr encodes the thyroid-stimulating hormone receptor (TSHR), a glycoprotein hormone GPCR primarily expressed in thyroid follicular cells that transduces TSH signals through Gs/adenylyl cyclase to elevate cAMP and activate PKA-dependent transcriptional programs. This signaling axis regulates thyroid hormone biosynthesis, iodide uptake, thyroglobulin processing, and follicular cell growth and differentiation. TSHR activity intersects with MAPK and PI3K pathways to coordinate proliferative and metabolic responses downstream of endocrine cues. Dysregulated Tshr signaling is implicated in autoimmune thyroid disease and thyroid functional abnormalities, making it a useful node for studying GPCR signaling, endocrine homeostasis, and immune-mediated receptor perturbation in mouse models.
TSHR CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Tshr gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Tshr 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 Tshr 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 TSHR protein expression.
This CRISPR knockout system enables efficient generation of Tshr-deficient cell models for investigation of TSHR signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Tshr exon(s) critical for TSHR 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 Tshr genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TSHR CRISPR/Cas9 KO Plasmid (m) and TSHR CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Tshr locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TSHR HDR Plasmid (m) and TSHR HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Tshr homology arms to support homology-directed repair at defined Tshr 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.