
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LSR CRISPR Activation Plasmid (h) | sc-401518-ACT | 20 µg | $397.00 |
Human LSR (lipolysis stimulated lipoprotein receptor), also known as angulin-1, is a membrane-associated protein that participates in lipid and lipoprotein handling and contributes to epithelial barrier organization at tricellular tight junctions. By coordinating junctional architecture and membrane trafficking, LSR influences cell polarity, paracellular permeability, and tissue homeostasis in barrier-forming epithelia. Altered LSR expression has been linked to dysregulated lipid metabolism and barrier dysfunction, processes relevant to inflammation, metabolic disorders, and tumor-associated changes in epithelial integrity. These functions position LSR as a useful node for studying cross-talk between lipid pathways and junctional signaling networks.
LSR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LSR expression without altering the underlying DNA sequence.
LSR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LSR 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 LSR transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous LSR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LSR locus and enabling the study of LSR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of LSR pathway restoration in tumor cells with silenced or reduced LSR expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.