IDH1 Lentiviral Activation Particles (m): sc-421022-LAC
- Target species: mouse
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- IDH1 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
- IDH1 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 IDH1 Lentiviral Activation Plasmid (m) and IDH1 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Idh1 promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IDH1 Lentiviral Activation Particles (m) | sc-421022-LAC | 200 µl | $455.00 |
Mouse Idh1 encodes the cytosolic NADP+-dependent isocitrate dehydrogenase IDH1, a key metabolic enzyme that converts isocitrate to α-ketoglutarate while generating NADPH. Through regulation of NADPH availability, IDH1 supports glutathione-based redox homeostasis, lipid biosynthesis, and cellular responses to oxidative stress, linking central carbon metabolism to antioxidant defenses. IDH1 activity influences α-ketoglutarate–dependent dioxygenase biology and can modulate epigenetic and hypoxia-associated signaling through metabolite balance. Dysregulation of Idh1 is therefore relevant to studies of metabolic rewiring, redox-driven phenotypes, and pathway crosstalk affecting proliferation and differentiation in mouse model systems.
IDH1 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 Idh1 upregulation across a broader range of human cell types.
IDH1 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 Idh1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous IDH1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Idh1 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.