TRH-R1 CRISPR/Cas9 KO Plasmid (m2): sc-423506-KO-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRH-R1 CRISPR/Cas9 Knockout (KO) Plasmid (m2) 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 TRH-R1 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 | |
TRH-R1 CRISPR/Cas9 KO Plasmid (m2) | sc-423506-KO-2 | 20 µg | $397.00 |
Overview
Trhr encodes thyrotropin-releasing hormone receptor 1 (TRH-R1), a class A GPCR that binds hypothalamic TRH to regulate pituitary-thyroid axis signaling and neuroendocrine control of metabolism. Upon ligand engagement, TRH-R1 primarily couples to Gq/11 to activate phospholipase C, driving IP3/DAG production, intracellular Ca2+ mobilization, and protein kinase C–dependent transcriptional programs. In the mouse, TRH-R1 signaling also interfaces with MAPK/ERK pathways and influences excitability and hormone secretion in TRH-responsive tissues. Dysregulation of TRH–TRH-R1 signaling has been linked to altered thyroid-stimulating hormone dynamics and broader endocrine and metabolic phenotypes, supporting its use in mechanistic studies of neuroendocrine homeostasis.
TRH-R1 CRISPR/Cas9 KO Plasmid (m2) is a pool of plasmids designed for targeted disruption of the Trhr gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trhr 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 Trhr 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 TRH-R1 protein expression.
This CRISPR knockout system enables efficient generation of Trhr-deficient cell models for investigation of TRH-R1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trhr exon(s) critical for TRH-R1 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 Trhr genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRH-R1 CRISPR/Cas9 KO Plasmid (m) and TRH-R1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trhr locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRH-R1 HDR Plasmid (m) and TRH-R1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trhr homology arms to support homology-directed repair at defined Trhr 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.