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.
NFKBIA/IkB alpha CRISPR Activation Plasmid (h): sc-400034-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NFKBIA/IkB alpha CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- NFKBIA/IkB alpha 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 NFKBIA/IkB alpha CRISPR Activation Plasmid (h) and NFKBIA/IkB alpha CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the NFKBIA 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: p-NFKBIA/IkB alpha Antibody (B-9): sc-8404
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NFKBIA/IkB alpha CRISPR Activation Plasmid (h) | sc-400034-ACT | 20 µg | $397.00 | |||
NFKBIA/IkB alpha CRISPR Activation Plasmid (h2) | sc-400034-ACT-2 | 20 µg | $397.00 |
NFKBIA encodes IκBα, a principal cytoplasmic inhibitor of NF-κB that binds RELA/p50 complexes and restricts their nuclear translocation under basal conditions. Upon stimulation by cytokines, Toll-like receptor ligands, or stress signals, IκBα is phosphorylated by the IKK complex, ubiquitinated, and degraded, enabling rapid NF-κB–dependent transcription of inflammatory, immune, and survival programs. NFKBIA also participates in negative-feedback control because it is itself an NF-κB target gene, helping reset pathway activity after signaling. Dysregulated NFKBIA expression or altered IκBα turnover has been linked to chronic inflammation, immune dysregulation, and NF-κB–driven tumor biology, making it a common node in studies of innate signaling and cell fate decisions.
NFKBIA/IkB alpha CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NFKBIA expression without altering the underlying DNA sequence.
NFKBIA/IkB alpha CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NFKBIA 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 NFKBIA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NFKBIA/IkB alpha expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NFKBIA locus and enabling the study of NFKBIA/IkB alpha-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NFKBIA/IkB alpha pathway restoration in tumor cells with silenced or reduced NFKBIA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.