
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRBP I CRISPR Activation Plasmid (h) | sc-402675-ACT | 20 µg | $397.00 |
RBP1 encodes cellular retinol-binding protein 1 (CRBP I), a cytosolic carrier that binds retinol and regulates its intracellular trafficking, storage, and metabolic conversion. By controlling delivery of retinol to retinol dehydrogenases and retinyl esterification machinery, CRBP I influences retinoid homeostasis and downstream retinoic acid–dependent transcriptional programs that shape epithelial differentiation, development, and metabolic regulation. Altered RBP1 expression has been associated with disrupted retinoid signaling in contexts such as epithelial transformation, fibrosis, and metabolic dysregulation, making it a useful node for studying vitamin A biology and transcriptional control. In human cells, CRBP I provides a tractable handle to interrogate how retinoid availability couples to nuclear receptor pathways and cell state transitions.
CRBP I CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RBP1 expression without altering the underlying DNA sequence.
CRBP I CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RBP1 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 RBP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CRBP I expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RBP1 locus and enabling the study of CRBP I-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CRBP I pathway restoration in tumor cells with silenced or reduced RBP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.