
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FANCA CRISPR Activation Plasmid (h) | sc-403205-ACT | 20 µg | $397.00 |
FANCA encodes a core component of the Fanconi anemia (FA) DNA repair pathway that coordinates the repair of DNA interstrand crosslinks and stabilizes replication forks during S phase. FANCA participates in the FA core complex that promotes monoubiquitination of FANCD2 and FANCI, enabling downstream nucleolytic processing and homologous recombination–associated repair. Disruption of FANCA compromises genome integrity, elevates chromosomal breakage, and sensitizes cells to crosslinking damage, linking this gene to the molecular pathology of Fanconi anemia and broader mechanisms of replication stress. As a result, FANCA is widely studied in pathways governing DNA damage signaling, cell-cycle checkpoints, and maintenance of chromosomal stability.
FANCA CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FANCA expression without altering the underlying DNA sequence.
FANCA CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FANCA 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 FANCA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FANCA expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FANCA locus and enabling the study of FANCA-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FANCA pathway restoration in tumor cells with silenced or reduced FANCA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.