TrkB CRISPR/Cas9 KO Plasmid (m): sc-421983
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TrkB 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 TrkB 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: TrkB Antibody (F-1): sc-377218
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TrkB CRISPR/Cas9 KO Plasmid (m) | sc-421983 | 20 µg | $397.00 |
Overview
Ntrk2 encodes the receptor tyrosine kinase TrkB, a high-affinity receptor for BDNF and NT-4/5 that regulates neuronal survival, differentiation, and synaptic plasticity. Upon ligand binding, TrkB activates canonical PI3K–AKT, MAPK/ERK, and PLCγ–Ca²⁺ signaling cascades that couple extracellular neurotrophin cues to transcriptional and cytoskeletal programs. TrkB-dependent signaling influences neurite outgrowth, dendritic spine remodeling, and activity-dependent circuit refinement in the developing and adult nervous system. Altered Ntrk2/TrkB pathway activity has been associated with neurodevelopmental and neuropsychiatric phenotypes as well as neurodegenerative processes, supporting its broad relevance in mechanisms-focused disease models.
TrkB CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ntrk2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ntrk2 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 Ntrk2 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 TrkB protein expression.
This CRISPR knockout system enables efficient generation of Ntrk2-deficient cell models for investigation of TrkB signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ntrk2 exon(s) critical for TrkB 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 Ntrk2 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TrkB CRISPR/Cas9 KO Plasmid (m) and TrkB CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ntrk2 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TrkB HDR Plasmid (m) and TrkB HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ntrk2 homology arms to support homology-directed repair at defined Ntrk2 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.