
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MC1-R CRISPR Activation Plasmid (h) | sc-402152-ACT | 20 µg | $397.00 |
MC1R encodes the melanocortin 1 receptor (MC1-R), a G protein–coupled receptor predominantly expressed in melanocytes where it regulates melanin synthesis and pigment switching. Upon binding melanocortins such as α-MSH, MC1-R activates adenylyl cyclase and cAMP/PKA signaling, promoting MITF-dependent transcriptional programs that support melanogenesis, DNA damage responses, and oxidative stress resilience. Variation or altered activity of MC1R is associated with pigmentation phenotypes and is widely studied in the context of UV-response biology and melanocyte transformation. These properties make MC1-R a useful node for interrogating GPCR signaling, cAMP-driven transcription, and pigment cell homeostasis in human cellular models.
MC1-R CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MC1R expression without altering the underlying DNA sequence.
MC1-R CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MC1R locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the MC1R transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MC1-R expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MC1R locus and enabling the study of MC1-R-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MC1-R pathway restoration in tumor cells with silenced or reduced MC1R expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.