
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Attractin CRISPR Activation Plasmid (h) | sc-406420-ACT | 20 µg | $397.00 | |||
Attractin CRISPR Activation Plasmid (h2) | sc-406420-ACT-2 | 20 µg | $397.00 |
Human ATRN encodes attractin, a transmembrane glycoprotein implicated in immune cell communication and inflammatory regulation, including roles in T cell–monocyte interactions and modulation of chemokine-driven cell adhesion. Attractin has been linked to melanocortin signaling biology through interactions with agouti-related pathways and is associated with processes that shape cell surface dynamics and extracellular ligand engagement. By influencing immune synapse behavior and leukocyte trafficking cues, ATRN is relevant to studies of neuroinflammation and immune dysregulation, and it is also investigated in contexts where altered cell–cell interactions contribute to disease phenotypes.
Attractin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ATRN expression without altering the underlying DNA sequence.
Attractin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ATRN 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 ATRN transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Attractin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ATRN locus and enabling the study of Attractin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Attractin pathway restoration in tumor cells with silenced or reduced ATRN expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.