JAB1 Lentiviral Activation Particles (m): sc-424107-LAC

Mouse Cops5 encodes JAB1 (also known as CSN5), the catalytic subunit of the COP9 signalosome that controls protein turnover by regulating cullin-RING ubiquitin ligases through deneddylation. By tuning ubiquitin-dependent degradation, JAB1 influences cell-cycle progression, DNA damage responses, and stress-adaptive transcriptional programs, including modulation of AP-1 activity and pathways linked to CDK inhibitor stability. JAB1 also interfaces with signaling and nuclear-cytoplasmic shuttling processes that affect proliferation and differentiation, making it relevant to models of dysregulated growth and inflammation-associated tissue remodeling. Altered CSN5/JAB1 activity has been associated with oncogenic pathway rewiring and immune signaling changes, supporting its utility in mechanistic studies of proteostasis and signaling cross-talk.

JAB1 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 Cops5 upregulation across a broader range of human cell types.

JAB1 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 Cops5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous JAB1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Cops5 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.