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.
RELA/NFκB p65 CRISPR Activation Plasmid (h): sc-400004-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RELA/NFκB p65 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- RELA/NFκB p65 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 RELA/NFκB p65 CRISPR Activation Plasmid (h) and RELA/NFκB p65 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the RELA 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: RELA/NFκB p65 Antibody (F-6): sc-8008
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RELA/NFκB p65 CRISPR Activation Plasmid (h) | sc-400004-ACT | 20 µg | $397.00 | |||
RELA/NFκB p65 CRISPR Activation Plasmid (h2) | sc-400004-ACT-2 | 20 µg | $397.00 |
RELA encodes the p65 subunit of NF-κB, a central transcription factor that controls inducible gene programs governing inflammation, innate and adaptive immune signaling, cell survival, and stress responses. Upon activation by pathways such as TNF receptor, IL-1 receptor, Toll-like receptors, and antigen receptor signaling, p65 forms dimers (commonly with NFKB1/p50), translocates to the nucleus, and regulates cytokines, chemokines, adhesion molecules, and anti-apoptotic factors. RELA activity is shaped by IκB-mediated cytoplasmic sequestration and stimulus-dependent post-translational modifications that tune chromatin engagement and transcriptional output. Dysregulated NF-κB/RELA signaling is frequently linked to chronic inflammatory states, oncogenic transcriptional programs, and microenvironmental interactions relevant to tumor progression and immune evasion.
RELA/NFκB p65 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RELA expression without altering the underlying DNA sequence.
RELA/NFκB p65 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RELA 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 RELA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RELA/NFκB p65 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RELA locus and enabling the study of RELA/NFκB p65-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RELA/NFκB p65 pathway restoration in tumor cells with silenced or reduced RELA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.