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.
N-CoR CRISPR Activation Plasmid (m): sc-422771-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- N-CoR CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- N-CoR CRISPR Activation Plasmid (m) 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 N-CoR CRISPR Activation Plasmid (m) and N-CoR CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Ncor1 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: N-CoR Antibody (F-1): sc-515934
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
N-CoR CRISPR Activation Plasmid (m) | sc-422771-ACT | 20 µg | $397.00 | |||
N-CoR CRISPR Activation Plasmid (m2) | sc-422771-ACT-2 | 20 µg | $397.00 |
Mouse Ncor1 encodes N-CoR (nuclear receptor corepressor 1), a scaffold corepressor that assembles HDAC3-containing chromatin remodeling complexes to enforce transcriptional repression at nuclear receptors and other sequence-specific transcription factors. Through regulation of histone acetylation and chromatin accessibility, N-CoR influences lineage specification, inflammatory gene programs, and metabolic homeostasis, integrating signaling from steroid/thyroid hormone receptors, Notch, and NF-κB-associated pathways. Altered NCOR1-dependent repression has been linked to dysregulated immune responses, neurodevelopmental phenotypes, and metabolic and oncogenic transcriptional states, making it a key node in epigenetic control of cell identity. As a conserved regulator of transcriptional networks, N-CoR is frequently studied in contexts such as macrophage activation, adipocyte biology, and differentiation-associated chromatin transitions.
N-CoR CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Ncor1 expression without altering the underlying DNA sequence.
N-CoR CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Ncor1 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 Ncor1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous N-CoR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Ncor1 locus and enabling the study of N-CoR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of N-CoR pathway restoration in tumor cells with silenced or reduced Ncor1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.