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.
NRSF CRISPR Activation Plasmid (h): sc-418578-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NRSF CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- NRSF 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 NRSF CRISPR Activation Plasmid (h) and NRSF CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the REST 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: NRSF Antibody (F-3): sc-374611
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NRSF CRISPR Activation Plasmid (h) | sc-418578-ACT | 20 µg | $397.00 | |||
NRSF CRISPR Activation Plasmid (h2) | sc-418578-ACT-2 | 20 µg | $397.00 |
RE1-silencing transcription factor (REST), also known as neuron-restrictive silencer factor (NRSF), is a zinc-finger transcriptional repressor that binds RE1/NRSE elements to regulate large gene networks controlling neuronal differentiation, synaptic function, and activity-dependent transcription. By recruiting corepressor complexes such as CoREST, HDACs, and chromatin-modifying enzymes, REST shapes epigenetic states and modulates RNA processing programs in neural and non-neural contexts. REST-dependent regulation intersects with chromatin remodeling, ion channel expression, and stress-response pathways that influence cell fate decisions and excitability. Dysregulated REST/NRSF activity has been implicated in neurodevelopmental and neurodegenerative phenotypes as well as tumor biology, supporting its use as a mechanistic node for studying transcriptional repression and neuronal gene circuitry in human cells.
NRSF CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous REST expression without altering the underlying DNA sequence.
NRSF CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the REST 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 REST transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NRSF expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native REST locus and enabling the study of NRSF-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NRSF pathway restoration in tumor cells with silenced or reduced REST expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.