RILP CRISPR Activation Plasmid (h): sc-402680-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RILP CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- RILP 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 RILP CRISPR Activation Plasmid (h) and RILP CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the RILP transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RILP CRISPR Activation Plasmid (h) | sc-402680-ACT | 20 µg | $397.00 |
RILP (Rab-interacting lysosomal protein) is a key effector of Rab7 that coordinates late endosome and lysosome positioning, maturation, and cargo trafficking along microtubules. By linking Rab7-positive membranes to the dynein–dynactin motor complex and participating in endosome–lysosome fusion events, RILP influences receptor downregulation, lysosomal degradation, and autophagic flux. These functions place RILP at the center of endolysosomal homeostasis and membrane trafficking pathways that shape signaling output and proteostasis. Dysregulation of Rab7–RILP–dependent transport has been associated with cellular stress responses and phenotypes relevant to neurodegeneration, infection biology, and cancer cell adaptation to altered lysosomal function.
RILP CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RILP expression without altering the underlying DNA sequence.
RILP CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RILP 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 RILP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RILP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RILP locus and enabling the study of RILP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RILP pathway restoration in tumor cells with silenced or reduced RILP expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.