
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FANCM CRISPR Activation Plasmid (h) | sc-403495-ACT | 20 µg | $397.00 |
Human FANCM encodes a DNA translocase that functions in the Fanconi anemia (FA) pathway to maintain genome stability during DNA replication stress. FANCM recognizes stalled replication forks and interstrand crosslinks, coordinating with the FA core complex, ATR-dependent checkpoint signaling, and homologous recombination factors to promote fork remodeling and repair. Through its roles in replication fork traverse, restart, and suppression of aberrant recombination, FANCM helps limit chromosome breakage and mutagenesis. Disruption of FANCM-mediated repair is linked to impaired crosslink repair capacity and genomic instability phenotypes relevant to Fanconi anemia biology and cancer-associated DNA damage response alterations.
FANCM CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FANCM expression without altering the underlying DNA sequence.
FANCM CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FANCM 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 FANCM transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FANCM expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FANCM locus and enabling the study of FANCM-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FANCM pathway restoration in tumor cells with silenced or reduced FANCM expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.