
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DAGLβ CRISPR Activation Plasmid (h) | sc-406084-ACT | 20 µg | $397.00 |
DAGLB encodes diacylglycerol lipase beta (DAGLβ), a serine hydrolase that converts diacylglycerol into 2-arachidonoylglycerol (2-AG), a major endocannabinoid lipid mediator. By controlling 2-AG availability, DAGLβ contributes to cannabinoid receptor signaling and coordinates lipid second-messenger flux with inflammatory and metabolic pathways. DAGLβ activity is frequently studied in immune cell activation, macrophage lipid signaling, and regulation of arachidonic acid–derived mediator production. Dysregulated endocannabinoid and eicosanoid networks involving DAGLβ have been linked to inflammatory states, neuroimmune crosstalk, and cardiometabolic phenotypes, supporting mechanistic research into disease-associated lipid signaling.
DAGLβ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DAGLB expression without altering the underlying DNA sequence.
DAGLβ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DAGLB 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 DAGLB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DAGLβ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DAGLB locus and enabling the study of DAGLβ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DAGLβ pathway restoration in tumor cells with silenced or reduced DAGLB expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.