ASC/TMS1/PYCARD Lentiviral Activation Particles (h): sc-400151-LAC

PYCARD encodes ASC (also known as TMS1), an adaptor protein that bridges pattern-recognition receptors to caspase-1 during inflammasome assembly. Through its PYD and CARD domains, ASC nucleates multimeric “ASC specks” to promote caspase-1 activation and downstream processing of IL-1β and IL-18, linking innate immune sensing to pyroptotic cell death. PYCARD-dependent signaling integrates with NLRP3, AIM2, and other inflammasome pathways, shaping inflammatory responses to infection and cellular stress. Dysregulated ASC activity has been implicated in chronic inflammatory and autoimmune conditions, neuroinflammation, and tumor-associated inflammation, making it a key target for mechanistic studies of innate immunity and cell death.

ASC/TMS1/PYCARD 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 PYCARD upregulation across a broader range of human cell types.

ASC/TMS1/PYCARD 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 PYCARD transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous ASC/TMS1/PYCARD expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PYCARD 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.