
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FANCL CRISPR Activation Plasmid (h) | sc-403812-ACT | 20 µg | $397.00 |
FANCL encodes an E3 ubiquitin-protein ligase that functions as a core catalytic component of the Fanconi anemia (FA) DNA repair pathway, coordinating repair of DNA interstrand crosslinks and replication-associated lesions. Within the FA core complex, FANCL mediates monoubiquitination of FANCD2 and FANCI, enabling recruitment of downstream nucleases and homologous recombination factors to stalled replication forks. This activity supports genome stability, S-phase checkpoint integrity, and cellular tolerance to genotoxic stress. Dysregulation of FANCL-dependent signaling is linked to Fanconi anemia biology, chromosomal instability, and DNA repair defects relevant to cancer and hematopoietic failure research.
FANCL CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FANCL expression without altering the underlying DNA sequence.
FANCL CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FANCL 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 FANCL transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FANCL expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FANCL locus and enabling the study of FANCL-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FANCL pathway restoration in tumor cells with silenced or reduced FANCL expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.