Skint8 Lentiviral Activation Particles (m2): sc-437039-LAC-2

Mouse Skint8 (selection and upkeep of intraepithelial T cells protein 8) is a member of the butyrophilin-like/Skint family implicated in epithelial immune regulation, with putative roles in shaping T cell selection and maintenance within barrier tissues such as skin. Skint proteins are generally linked to cell–cell interaction and antigen receptor–dependent signaling programs that influence thymic and peripheral lymphocyte differentiation, contributing to tissue-resident immune homeostasis. Dysregulation of Skint-family pathways is relevant to studies of cutaneous inflammation, host defense at epithelial surfaces, and immune surveillance mechanisms. Skint8 is therefore a useful target for gene editing to interrogate epithelial–immune crosstalk, map tissue-resident T cell developmental cues, and model how barrier-associated immunoregulatory networks impact inflammatory phenotypes in mouse systems.

Skint8 Lentiviral Activation Particles (m2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Skint8 upregulation across a broader range of human cell types.

Skint8 Lentiviral Activation Particles (m2) 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 Skint8 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Skint8 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Skint8 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.