MC1-R CRISPR/Cas9 KO Plasmid (h): sc-402152
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MC1-R 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 MC1-R 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: MC1-R Antibody (578CT6.2.3): sc-517344
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MC1-R CRISPR/Cas9 KO Plasmid (h) | sc-402152 | 20 µg | $397.00 |
Overview
MC1R encodes melanocortin 1 receptor (MC1-R), a G protein–coupled receptor predominantly expressed in melanocytes that couples to Gαs to stimulate adenylate cyclase and elevate cAMP. Activated MC1-R signaling promotes eumelanin synthesis and supports pigmentation programs through downstream regulators such as MITF, while intersecting with cellular stress responses including oxidative and UV-induced damage pathways. Variation or dysregulation of MC1R is linked to altered pigment phenotypes and has been widely studied for its association with melanoma susceptibility and other UV-related skin pathologies. Beyond pigmentation, MC1-R signaling is also investigated in inflammation and melanocortin network biology, providing a mechanistic entry point for receptor signaling and GPCR pathway research.
MC1-R CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MC1R gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MC1R 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 MC1R 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 MC1-R protein expression.
This CRISPR knockout system enables efficient generation of MC1R-deficient cell models for investigation of MC1-R signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting MC1R exon(s) critical for MC1-R 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 MC1R genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by MC1-R CRISPR/Cas9 KO Plasmid (h) and MC1-R CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MC1R locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by MC1-R HDR Plasmid (h) and MC1-R HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MC1R homology arms to support homology-directed repair at defined MC1R 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.