
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ANKRD22 Lentiviral Activation Particles (h) | sc-416874-LAC | 200 µl | $455.00 |
Human ANKRD22 encodes an ankyrin repeat–containing protein implicated in protein–protein interaction networks that influence cellular growth control and metabolic adaptation. Reported expression changes across tumor types suggest ANKRD22 can be associated with proliferative signaling and stress-response programs, potentially intersecting with pathways governing mitochondrial activity, cytoskeletal organization, and transcriptional regulation. As an ankyrin repeat protein, ANKRD22 is positioned to modulate pathway crosstalk by scaffolding regulatory complexes rather than acting as an enzyme. These features make ANKRD22 a useful target for dissecting gene regulation and context-dependent phenotypes in cancer biology and cell state transitions.
ANKRD22 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 ANKRD22 upregulation across a broader range of human cell types.
ANKRD22 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 ANKRD22 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ANKRD22 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ANKRD22 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.