
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DAGLα CRISPR Activation Plasmid (h) | sc-402826-ACT | 20 µg | $397.00 | |||
DAGLα CRISPR Activation Plasmid (h2) | sc-402826-ACT-2 | 20 µg | $397.00 |
DAGLA encodes diacylglycerol lipase alpha (DAGLα), a membrane-associated serine hydrolase that converts sn-1-acyl-2-arachidonoyl glycerol into 2-arachidonoylglycerol (2-AG), a major endocannabinoid lipid mediator. By controlling 2-AG production at synapses and in other signaling microdomains, DAGLα regulates retrograde cannabinoid signaling through CB1/CB2 receptors and integrates with phosphoinositide and diacylglycerol-driven pathways. This enzyme influences neuronal excitability, synaptic plasticity, and neuroinflammatory signaling, and altered endocannabinoid tone has been linked to multiple neurological and neuropsychiatric disease contexts. DAGLα activity also intersects with arachidonic acid-derived lipid networks, making DAGLA a useful node for studying lipid signaling homeostasis and stimulus-coupled signal transduction.
DAGLα CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DAGLA expression without altering the underlying DNA sequence.
DAGLα CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DAGLA 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 DAGLA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DAGLα expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DAGLA locus and enabling the study of DAGLα-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DAGLα pathway restoration in tumor cells with silenced or reduced DAGLA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.