LTK CRISPR/Cas9 KO Plasmid (m): sc-421486
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LTK 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 LTK 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: LTK Antibody (B-6): sc-393465
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LTK CRISPR/Cas9 KO Plasmid (m) | sc-421486 | 20 µg | $397.00 |
Overview
Mouse Ltk encodes leukocyte tyrosine kinase (LTK), a receptor tyrosine kinase that regulates signal transduction controlling cell growth, survival, and differentiation. LTK autophosphorylation can engage downstream kinase cascades, including MAPK/ERK and PI3K/AKT-associated signaling, influencing cellular proliferation and stress-response programs. In immune and nervous system contexts, LTK has been linked to lineage specification and functional maturation, making it relevant for studying receptor tyrosine kinase network crosstalk and developmental signaling. Dysregulated RTK signaling, including alterations in LTK activity, is frequently examined in models of aberrant proliferation and transformation, supporting its use in mechanistic studies of disease-associated signaling circuitry.
LTK CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ltk gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ltk 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 Ltk 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 LTK protein expression.
This CRISPR knockout system enables efficient generation of Ltk-deficient cell models for investigation of LTK signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ltk exon(s) critical for LTK 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 Ltk genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LTK CRISPR/Cas9 KO Plasmid (m) and LTK CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ltk locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LTK HDR Plasmid (m) and LTK HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ltk homology arms to support homology-directed repair at defined Ltk 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.