betaKlotho Lentiviral Activation Particles (h): sc-401614-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- betaKlotho 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
- betaKlotho 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 betaKlotho Lentiviral Activation Plasmid (h) and betaKlotho Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the KLB promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
betaKlotho Lentiviral Activation Particles (h) | sc-401614-LAC | 200 µl | $455.00 |
Human KLB encodes betaKlotho, a single-pass transmembrane co-receptor that confers ligand specificity to endocrine FGF signaling, most prominently FGF19/FGF15 and FGF21. By forming receptor complexes with FGFRs, betaKlotho regulates MAPK/ERK and PI3K/AKT-linked transcriptional programs controlling bile acid homeostasis, lipid and glucose metabolism, and energy balance. KLB expression is enriched in metabolic tissues such as liver and adipose, where it shapes nutrient-responsive signaling and endocrine crosstalk. Altered betaKlotho activity or expression has been associated with metabolic dysregulation and related disease biology, making KLB a key node for mechanistic studies of hepatometabolic pathways.
betaKlotho 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 KLB upregulation across a broader range of human cell types.
betaKlotho 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 KLB transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous betaKlotho expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native KLB 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.