MISP Lentiviral Activation Particles (h): sc-409029-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- MISP Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- MISP Lentiviral Activation Particles (h) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by MISP Lentiviral Activation Plasmid (h) and MISP Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the MISP promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MISP Lentiviral Activation Particles (h) | sc-409029-LAC | 200 µl | $455.00 |
Human MISP (mitotic spindle positioning) encodes an actin- and microtubule-associated protein that localizes to spindle poles and the cell cortex to help orient the mitotic spindle and support accurate chromosome segregation. Through interactions with cytoskeletal regulators and centrosomal components, MISP contributes to mitotic progression, cytokinesis, and maintenance of epithelial architecture. Dysregulation of spindle positioning and division symmetry links MISP-associated pathways to genome instability and altered cell polarity, processes frequently interrogated in studies of tumor biology and proliferative stress. As a node connecting cortical actin dynamics with microtubule organization, MISP is relevant to investigations of cell cycle control, aneuploidy, and tissue organization.
MISP 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 MISP upregulation across a broader range of human cell types.
MISP 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 MISP transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MISP expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MISP 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.