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.
RIP140 CRISPR Activation Plasmid (h): sc-401787-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RIP140 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- RIP140 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 RIP140 CRISPR Activation Plasmid (h) and RIP140 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the NRIP1 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: RIP140 Antibody (2656C6a): sc-81370
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RIP140 CRISPR Activation Plasmid (h) | sc-401787-ACT | 20 µg | $397.00 |
NRIP1 encodes RIP140, a transcriptional coregulator that modulates gene expression by interacting with nuclear receptors and other DNA-binding transcription factors to coordinate metabolic and endocrine programs. RIP140 influences adipogenesis, mitochondrial function, lipid and glucose homeostasis, and inflammatory signaling by shaping chromatin-dependent activation or repression at target promoters. Through crosstalk with pathways such as estrogen receptor signaling, PPAR-dependent transcription, and broader coactivator/corepressor networks, RIP140 helps integrate nutrient cues with cellular differentiation and stress responses. Dysregulated NRIP1/RIP140 activity has been associated in the literature with metabolic dysfunction, reproductive phenotypes, and altered transcriptional states observed in several disease-relevant contexts, supporting its use in mechanistic studies.
RIP140 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NRIP1 expression without altering the underlying DNA sequence.
RIP140 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NRIP1 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 NRIP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RIP140 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NRIP1 locus and enabling the study of RIP140-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RIP140 pathway restoration in tumor cells with silenced or reduced NRIP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.