
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LYVE-1 CRISPR Activation Plasmid (h) | sc-401446-ACT | 20 µg | $397.00 |
LYVE1 encodes lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), a type I membrane glycoprotein that binds hyaluronan and contributes to lymphatic endothelial identity, extracellular matrix interactions, and leukocyte trafficking. LYVE-1 is commonly used as a marker of lymphatic endothelium and can also be detected in specialized macrophage populations, supporting studies of tissue fluid homeostasis and immune cell migration. Through hyaluronan-dependent adhesion and endocytosis-related processes, LYVE-1 links glycocalyx remodeling to vascular and stromal microenvironment dynamics. Dysregulated LYVE1 expression patterns are investigated in contexts involving lymphangiogenesis, chronic inflammation, and tumor-associated lymphatic remodeling, informing mechanistic research on metastasis-associated routes without implying clinical outcomes.
LYVE-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LYVE1 expression without altering the underlying DNA sequence.
LYVE-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LYVE1 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 LYVE1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous LYVE-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LYVE1 locus and enabling the study of LYVE-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of LYVE-1 pathway restoration in tumor cells with silenced or reduced LYVE1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.