Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ABHD14B CRISPR Activation Plasmid (h): sc-410211-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABHD14B CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ABHD14B CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by ABHD14B CRISPR Activation Plasmid (h) and ABHD14B CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ABHD14B transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ABHD14B Antibody (E-12): sc-515084
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABHD14B CRISPR Activation Plasmid (h) | sc-410211-ACT | 20 µg | $397.00 | |||
ABHD14B CRISPR Activation Plasmid (h2) | sc-410211-ACT-2 | 20 µg | $397.00 |
Human ABHD14B (abhydrolase domain containing 14B) encodes a serine hydrolase–family protein predicted to participate in lipid and small-molecule metabolism through hydrolytic activity, contributing to cellular homeostasis and stress-responsive signaling. As a member of the α/β-hydrolase superfamily, ABHD14B is broadly linked to pathways that regulate membrane lipid remodeling, mitochondrial function, and redox balance, processes that can influence proliferation and inflammatory responses. Altered expression of hydrolases in this class has been associated with metabolic dysregulation and tumor biology, making ABHD14B a useful target for mechanistic studies in systems where lipid handling and bioenergetics are perturbed. Functional interrogation of ABHD14B supports research into how enzymatic control of lipid-derived signals interfaces with transcriptional programs and cell-state transitions.
ABHD14B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ABHD14B expression without altering the underlying DNA sequence.
ABHD14B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ABHD14B 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 ABHD14B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ABHD14B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ABHD14B locus and enabling the study of ABHD14B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ABHD14B pathway restoration in tumor cells with silenced or reduced ABHD14B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.