TRH CRISPR/Cas9 KO Plasmid (m): sc-423505
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRH 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 TRH 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 CRISPR/Cas9 KO Plasmid (m) | sc-423505 | 20 µg | $397.00 |
Overview
Trh encodes thyrotropin-releasing hormone (TRH), a hypothalamic neuropeptide synthesized as a preprohormone and processed into bioactive TRH that signals through TRH receptors to regulate the hypothalamic–pituitary–thyroid axis. TRH integrates neuroendocrine control of pituitary thyrotropin release and influences broader homeostatic processes including energy balance, thermoregulation, and neurobehavioral circuits. In the CNS, TRHergic neurons interface with neurotransmitter systems and stress-responsive pathways, linking peptide signaling to neuronal excitability and endocrine feedback. Dysregulation of TRH signaling has been associated with alterations in thyroid hormone homeostasis and phenotypes relevant to metabolic and neuroendocrine disorders, making Trh a useful target for mechanistic studies in mouse models.
TRH CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trh gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trh 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 Trh 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 protein expression.
This CRISPR knockout system enables efficient generation of Trh-deficient cell models for investigation of TRH signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trh exon(s) critical for TRH 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 Trh genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRH CRISPR/Cas9 KO Plasmid (m) and TRH CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trh locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRH HDR Plasmid (m) and TRH HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trh homology arms to support homology-directed repair at defined Trh 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.