
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATR CRISPR Activation Plasmid (m) | sc-434115-ACT | 20 µg | $397.00 |
Mouse Atr encodes ATR, a PI3K-like serine/threonine kinase that coordinates the DNA damage response during replication stress. ATR is activated at RPA-coated single-stranded DNA and signals through effectors such as CHK1 to stabilize stalled replication forks, regulate origin firing, and enforce intra-S and G2/M checkpoints. This pathway preserves genome integrity by promoting DNA repair and controlling cell-cycle progression, intersecting with processes including homologous recombination, replication fork protection, and apoptosis regulation. Dysregulated ATR signaling is linked to genomic instability phenotypes and is widely studied in the context of cancer biology and developmental disorders associated with impaired DNA damage checkpoint control.
ATR CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Atr expression without altering the underlying DNA sequence.
ATR CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Atr 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 Atr transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ATR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Atr locus and enabling the study of ATR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ATR pathway restoration in tumor cells with silenced or reduced Atr expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.