Klotho Lentiviral Activation Particles (m): sc-421290-LAC
- Target species: mouse
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- Klotho Lentiviral Activation Particles (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- Klotho Lentiviral Activation Particles (m) 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 Klotho Lentiviral Activation Plasmid (m) and Klotho Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Kl promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: Klotho Antibody (A-9): sc-515942
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Klotho Lentiviral Activation Particles (m) | sc-421290-LAC | 200 µl | $455.00 |
Mouse Kl encodes Klotho, a type I single-pass transmembrane protein whose extracellular domain can be shed to act as a circulating factor that modulates growth factor and hormone signaling. Klotho functions as an obligate co-receptor for endocrine FGF signaling (notably FGF23) to regulate phosphate and vitamin D metabolism, and it also influences oxidative stress responses and ion channel/transport processes in multiple tissues. Altered Kl/Klotho expression is linked to dysregulated mineral homeostasis, renal and cardiovascular phenotypes, and age-associated functional decline in mouse models, making it a widely used node for pathway interrogation. At the cellular level, Klotho impacts transcriptional and signaling programs connected to metabolic regulation, inflammatory tone, and stress resilience, supporting mechanistic studies of degeneration-associated biology.
Klotho 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 Kl upregulation across a broader range of human cell types.
Klotho 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 Kl transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Klotho expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Kl 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.