LRSAM1 CRISPR/Cas9 KO Plasmid (h): sc-407099
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRSAM1 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 LRSAM1 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 | |
LRSAM1 CRISPR/Cas9 KO Plasmid (h) | sc-407099 | 20 µg | $397.00 |
Overview
LRSAM1 (leucine rich repeat and sterile alpha motif containing 1) encodes a cytosolic RING-type E3 ubiquitin ligase that contributes to ubiquitin-dependent protein quality control and endosomal trafficking through interactions with TSG101 and other components of the ESCRT machinery. By regulating ubiquitination and turnover of specific substrates, LRSAM1 influences intracellular sorting, membrane dynamics, and neuronal homeostasis. Disruption of LRSAM1 function has been linked to peripheral neuropathy, including Charcot–Marie–Tooth disease type 2P, highlighting its relevance to axonal maintenance and proteostasis pathways. LRSAM1 is therefore of interest for studies of ubiquitin signaling, vesicle trafficking, and neurodegeneration-associated cellular stress responses.
LRSAM1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the LRSAM1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the LRSAM1 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 LRSAM1 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 LRSAM1 protein expression.
This CRISPR knockout system enables efficient generation of LRSAM1-deficient cell models for investigation of LRSAM1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting LRSAM1 exon(s) critical for LRSAM1 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 LRSAM1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LRSAM1 CRISPR/Cas9 KO Plasmid (h) and LRSAM1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the LRSAM1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LRSAM1 HDR Plasmid (h) and LRSAM1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by LRSAM1 homology arms to support homology-directed repair at defined LRSAM1 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.