MaxiKα Lentiviral Activation Particles (h): sc-402208-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- MaxiKα 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
- MaxiKα 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 MaxiKα Lentiviral Activation Plasmid (h) and MaxiKα Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the KCNMA1 promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: MaxiKα Antibody (B-1): sc-374142
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MaxiKα Lentiviral Activation Particles (h) | sc-402208-LAC | 200 µl | $455.00 |
KCNMA1 encodes the pore-forming α subunit of the large-conductance, calcium- and voltage-activated potassium channel MaxiKα (BK). This channel couples intracellular Ca²⁺ signals and membrane depolarization to K⁺ efflux, shaping action potential repolarization, firing frequency, and afterhyperpolarization in excitable tissues. MaxiKα activity integrates with Ca²⁺-dependent signaling and ion homeostasis pathways to regulate smooth muscle tone, neuronal excitability, and secretion. Dysregulated KCNMA1 function or expression has been linked to disorders involving altered excitability and contractility, including neurodevelopmental phenotypes, seizure susceptibility, and vascular or airway smooth muscle dysfunction, supporting mechanistic studies in relevant cellular models.
MaxiKα 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 KCNMA1 upregulation across a broader range of human cell types.
MaxiKα 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 KCNMA1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MaxiKα expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native KCNMA1 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.