LEPROT CRISPR/Cas9 KO Plasmid (h): sc-406321
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LEPROT 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 LEPROT 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 | |
LEPROT CRISPR/Cas9 KO Plasmid (h) | sc-406321 | 20 µg | $397.00 |
Overview
LEPROT (leptin receptor overlapping transcript), also known as endospanin-1, is an endosomal membrane protein that modulates the trafficking and cell-surface abundance of cytokine receptors, with prominent effects on LEPR and related signaling complexes. By regulating receptor internalization and recycling, LEPROT can influence pathway output in JAK/STAT signaling and broader membrane-proximal control of signal transduction. Altered LEPROT expression has been linked to metabolic phenotypes through impacts on leptin responsiveness and energy homeostasis. Its role in receptor sorting also makes it relevant to studies of inflammation-associated signaling and dysregulated receptor turnover in disease contexts.
LEPROT CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the LEPROT gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the LEPROT 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 LEPROT 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 LEPROT protein expression.
This CRISPR knockout system enables efficient generation of LEPROT-deficient cell models for investigation of LEPROT signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting LEPROT exon(s) critical for LEPROT 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 LEPROT genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by LEPROT CRISPR/Cas9 KO Plasmid (h) and LEPROT CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the LEPROT locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by LEPROT HDR Plasmid (h) and LEPROT HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by LEPROT homology arms to support homology-directed repair at defined LEPROT 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.