LSD1 Lentiviral Activation Particles (m): sc-430289-LAC
- Target species: mouse
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- LSD1 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
- LSD1 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 LSD1 Lentiviral Activation Plasmid (m) and LSD1 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Kdm1a promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: LSD1 Antibody (B-9): sc-271720
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LSD1 Lentiviral Activation Particles (m) | sc-430289-LAC | 200 µl | $455.00 |
Mouse Kdm1a encodes lysine-specific demethylase 1A (LSD1), a FAD-dependent chromatin regulator that removes mono- and di-methyl marks from histone H3K4 and H3K9 to modulate transcriptional programs. LSD1 functions in repressive and activating complexes such as CoREST and NuRD, integrating with RNA polymerase II control, enhancer dynamics, and lineage-specific transcription factor networks to regulate differentiation, cell-cycle progression, and metabolic state. Through these epigenetic pathways, Kdm1a influences hematopoietic and neural development and contributes to aberrant transcriptional circuits relevant to cancer biology and neurodevelopmental phenotypes. Its central role in chromatin remodeling makes Kdm1a a key node for studying epigenetic control of gene expression in mouse models.
LSD1 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 Kdm1a upregulation across a broader range of human cell types.
LSD1 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 Kdm1a transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous LSD1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Kdm1a 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.