
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATAD5 CRISPR Activation Plasmid (h) | sc-405654-ACT | 20 µg | $397.00 | |||
ATAD5 CRISPR Activation Plasmid (h2) | sc-405654-ACT-2 | 20 µg | $397.00 |
Human ATAD5 encodes an AAA+ ATPase that regulates genome stability by promoting PCNA unloading from chromatin during DNA replication and repair. Through this role, ATAD5 helps coordinate replication fork progression, post-replication repair, and resolution of replication stress, intersecting with pathways that preserve DNA integrity during S phase. Perturbation of ATAD5 activity can elevate replication-associated DNA damage and chromosomal instability, processes frequently examined in cancer biology and other disorders linked to defective DNA damage responses. ATAD5 is therefore widely used as a mechanistic entry point for studying replication-coupled repair and checkpoint signaling in mammalian cells.
ATAD5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ATAD5 expression without altering the underlying DNA sequence.
ATAD5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ATAD5 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 ATAD5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ATAD5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ATAD5 locus and enabling the study of ATAD5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ATAD5 pathway restoration in tumor cells with silenced or reduced ATAD5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.