AHNAK Lentiviral Activation Particles (m): sc-425992-LAC

Ahnak encodes AHNAK, a large scaffold protein that associates with the plasma membrane and cytoskeleton to coordinate cell architecture, adhesion, and signal integration. In mouse cells, AHNAK has been linked to calcium handling and membrane repair processes, and it can modulate pathways that converge on cytoskeletal remodeling, including PKC- and TGF-β-associated signaling. Through these functions, AHNAK contributes to regulation of cell migration and differentiation, making it relevant to studies of tissue remodeling and stress responses. Altered AHNAK expression or localization has been reported in multiple disease contexts, supporting its use as a mechanistic node for dissecting signaling–structure relationships in biomedical research models.

AHNAK 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 Ahnak upregulation across a broader range of human cell types.

AHNAK 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 Ahnak transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous AHNAK expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Ahnak 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.