FANCB CRISPR Activation Plasmid (h): sc-417439-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- FANCB CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- FANCB 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 FANCB CRISPR Activation Plasmid (h) and FANCB CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the FANCB transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FANCB CRISPR Activation Plasmid (h) | sc-417439-ACT | 20 µg | $397.00 |
FANCB encodes a core component of the Fanconi anemia (FA) DNA repair pathway that safeguards genome integrity during S phase by promoting repair of DNA interstrand crosslinks. Within the FA core complex, FANCB supports assembly and activity of the E3 ubiquitin ligase module that monoubiquitinates FANCD2 and FANCI, enabling downstream coordination with homologous recombination and replication fork protection mechanisms. Disruption or dysfunction of FANCB compromises the FA/BRCA network, elevating replication stress, chromosome instability, and sensitivity to crosslinking damage. Pathogenic variation in FANCB is associated with Fanconi anemia and related developmental and bone marrow failure phenotypes, making FANCB regulation a useful handle for studying DNA damage responses.
FANCB CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FANCB expression without altering the underlying DNA sequence.
FANCB CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FANCB 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 FANCB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FANCB expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FANCB locus and enabling the study of FANCB-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FANCB pathway restoration in tumor cells with silenced or reduced FANCB expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.