
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ATR Lentiviral Activation Particles (m) | sc-434115-LAC | 200 µl | $455.00 |
Mouse Atr encodes ATR, a PI3K-like serine/threonine kinase that orchestrates the DNA damage response to replication stress and single-stranded DNA. ATR is activated through ATRIP and TOPBP1-dependent recruitment and signals primarily via CHK1 to stabilize stalled replication forks, regulate origin firing, and coordinate S and G2/M checkpoint control. This pathway interfaces with Fanconi anemia components, homologous recombination factors, and cell cycle regulators to preserve genome integrity. Disruption or dysregulation of ATR signaling is widely used to model mechanisms underlying genomic instability, replication-associated DNA lesions, and stress-adaptive proliferative programs relevant to cancer biology and developmental phenotypes in mouse systems.
ATR Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Atr upregulation across a broader range of human cell types.
ATR Lentiviral Activation Particles (m) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Atr transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ATR expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Atr genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.