Lck BP-1 CRISPR/Cas9 KO Plasmid (m): sc-420811
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Lck BP-1 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 Lck BP-1 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 | |
Lck BP-1 CRISPR/Cas9 KO Plasmid (m) | sc-420811 | 20 µg | $397.00 |
Overview
Hcls1 encodes hematopoietic cell–specific Lyn substrate 1 (Lck BP-1) in mouse, an adaptor protein enriched in immune lineages that couples antigen receptor signaling to cytoskeletal remodeling. Through phosphorylation-dependent interactions with Src family kinases and actin-regulatory complexes, Lck BP-1 contributes to immunoreceptor-driven calcium flux, MAPK activation, and dynamic changes in cell shape and motility. This signaling node influences lymphocyte activation, adhesion, and trafficking, linking receptor proximal events to downstream transcriptional responses. Dysregulation of Hcls1-associated pathways is relevant to studies of inflammatory signaling, aberrant immune cell activation, and hematopoietic cell biology.
Lck BP-1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Hcls1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Hcls1 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 Hcls1 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 Lck BP-1 protein expression.
This CRISPR knockout system enables efficient generation of Hcls1-deficient cell models for investigation of Lck BP-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Hcls1 exon(s) critical for Lck BP-1 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 Hcls1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Lck BP-1 CRISPR/Cas9 KO Plasmid (m) and Lck BP-1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Hcls1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Lck BP-1 HDR Plasmid (m) and Lck BP-1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Hcls1 homology arms to support homology-directed repair at defined Hcls1 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.