Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
USP34 Lentiviral Activation Particles (h): sc-409215-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- USP34 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
- USP34 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 USP34 Lentiviral Activation Plasmid (h) and USP34 Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the USP34 promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: USP34 Antibody (3H9): sc-100631
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
USP34 Lentiviral Activation Particles (h) | sc-409215-LAC | 200 µl | $455.00 |
Human USP34 encodes a ubiquitin-specific protease that removes ubiquitin chains from substrate proteins to modulate their stability, localization, and signaling output. USP34 has been implicated in regulation of Wnt/β-catenin pathway dynamics through deubiquitination of pathway components, thereby influencing transcriptional programs that govern proliferation, differentiation, and stem-like cell states. It also participates in cellular proteostasis and stress-response processes by tuning ubiquitin-dependent turnover and signaling crosstalk. Dysregulated USP34 activity or expression has been associated with altered oncogenic signaling and genome maintenance phenotypes, making it relevant for mechanistic studies in cancer biology and related signaling-driven disorders.
USP34 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 USP34 upregulation across a broader range of human cell types.
USP34 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 USP34 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous USP34 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native USP34 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.