Siglec-9 Lentiviral Activation Particles (h): sc-406675-LAC

SIGLEC9 encodes Siglec-9, an inhibitory sialic acid–binding immunoglobulin-like lectin predominantly expressed on neutrophils, monocytes, and subsets of NK cells. Through ITIM-dependent signaling and recruitment of phosphatases such as SHP-1/2, Siglec-9 dampens activating receptor pathways to modulate leukocyte activation, cytokine output, and cytotoxic responses in the context of sialylated self-associated molecular patterns. This checkpoint-like regulation influences cell–cell interactions, adhesion, and inflammatory resolution at mucosal and tumor-associated microenvironments. Dysregulated SIGLEC9 activity has been linked to altered innate immune surveillance and inflammatory phenotypes, supporting its study in immune evasion mechanisms and myeloid/NK functional polarization.

Siglec-9 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 SIGLEC9 upregulation across a broader range of human cell types.

Siglec-9 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 SIGLEC9 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Siglec-9 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SIGLEC9 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.