Atm Lentiviral Activation Particles (h): sc-400192-LAC

Human ATM encodes the Atm serine/threonine kinase, a central regulator of the DNA damage response that is rapidly activated by double-strand breaks. Atm coordinates checkpoint signaling through phosphorylation of key substrates including TP53, H2AX, CHEK2, and KAP1/TRIM28, integrating repair pathway choice, replication stress responses, and cell-cycle control. This signaling network interfaces with homologous recombination, non-homologous end joining, and chromatin remodeling to preserve genome stability. Altered ATM function is strongly linked to radiosensitivity and cancer predisposition biology, making ATM a widely used node for studying genome maintenance, stress signaling, and tumor suppressor pathways in human cells.

Atm Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient ATM upregulation across a broader range of human cell types.

Atm Lentiviral Activation Particles (h) 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 ATM transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Atm expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ATM 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.