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.
NGAL CRISPR Activation Plasmid (h): sc-401838-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NGAL CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- NGAL 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 NGAL CRISPR Activation Plasmid (h) and NGAL CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the LCN2 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: NGAL Antibody (H-4): sc-518095
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NGAL CRISPR Activation Plasmid (h) | sc-401838-ACT | 20 µg | $397.00 |
LCN2 encodes neutrophil gelatinase-associated lipocalin (NGAL), a secreted lipocalin that binds siderophore–iron complexes and modulates iron trafficking, antimicrobial defense, and epithelial stress responses. NGAL participates in innate immune signaling and inflammatory programs, including crosstalk with NF-κB- and cytokine-driven pathways, and is frequently induced by tissue injury and cellular stress. In human biology, altered LCN2/NGAL expression has been linked to dysregulated inflammation, metabolic remodeling, and tumor-associated microenvironment changes, making it a useful marker and mechanistic node for studying immune–epithelial interactions. Its roles in extracellular matrix dynamics and protease-associated processes further connect NGAL to contexts such as barrier dysfunction and remodeling phenotypes.
NGAL CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LCN2 expression without altering the underlying DNA sequence.
NGAL CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LCN2 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 LCN2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NGAL expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LCN2 locus and enabling the study of NGAL-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NGAL pathway restoration in tumor cells with silenced or reduced LCN2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.