SID-2 Lentiviral Activation Particles (h): sc-407959-LAC

SIDT2 (SID-2) encodes a lysosomal/endolysosomal membrane protein implicated in nucleic acid handling within the endocytic pathway, including uptake and intracellular trafficking of extracellular double-stranded RNA and related oligonucleotide species. By coupling membrane transport with lysosomal homeostasis, SID-2 has been linked to processes such as vesicular maturation, autophagy–lysosome function, and innate immune sensing pathways that respond to aberrant nucleic acids. Altered SIDT2 activity has been associated with dysregulated lysosomal storage and inflammatory signaling, making it relevant to studies of neurodegeneration, metabolic dysfunction, and host–pathogen interactions. These connections position SIDT2 as a useful node for dissecting endosomal trafficking and nucleic acid–driven stress responses in human cells.

SID-2 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 SIDT2 upregulation across a broader range of human cell types.

SID-2 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 SIDT2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous SID-2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SIDT2 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.