
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FBP1 CRISPR Activation Plasmid (h) | sc-401293-ACT | 20 µg | $397.00 |
Human FUBP1 encodes far upstream element-binding protein 1 (FBP1), a single-stranded nucleic acid–binding regulator that modulates transcriptional and post-transcriptional programs by interacting with promoter-associated elements and RNA targets. FBP1 is best known for influencing MYC expression and broader gene networks that govern cell-cycle progression, proliferation, and stress-adaptive responses. Through these activities, FUBP1 connects to pathways controlling chromatin-associated transcriptional regulation and RNA metabolism, making it a key node for studying context-dependent gene expression. Altered FUBP1 activity or dosage has been reported in multiple cancer- and neurodevelopment-relevant settings, supporting its use in mechanistic models of oncogenic signaling, differentiation, and genome stability.
FBP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FUBP1 expression without altering the underlying DNA sequence.
FBP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FUBP1 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 FUBP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FBP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FUBP1 locus and enabling the study of FBP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FBP1 pathway restoration in tumor cells with silenced or reduced FUBP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.