TET1 Lentiviral Activation Particles (h2): sc-400845-LAC-2
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- TET1 Lentiviral Activation Particles (h2) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- TET1 Lentiviral Activation Particles (h2) 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 TET1 Lentiviral Activation Plasmid (h2) and TET1 Lentiviral Activation Plasmid (h22) target distinct regulatory regions of the TET1 promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: TET1 Antibody (4F4): sc-293186
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TET1 Lentiviral Activation Particles (h2) | sc-400845-LAC-2 | 200 µl | $455.00 |
Human TET1 (ten-eleven translocation 1) encodes an Fe(II)/2-oxoglutarate–dependent dioxygenase that catalyzes iterative oxidation of 5-methylcytosine to 5-hydroxymethylcytosine and further oxidized derivatives, promoting active DNA demethylation and epigenetic remodeling. TET1 activity shapes transcriptional programs through regulation of CpG island methylation, enhancer dynamics, and chromatin state, interfacing with DNA repair and replication-associated maintenance of genome integrity. Dysregulated TET1 expression or function is linked to aberrant DNA methylation landscapes observed in cancer and neurodevelopmental and neurodegenerative contexts, making it a key node in studies of epigenome stability. Gene editing of TET1 supports mechanistic dissection of DNA methylation turnover, lineage specification and pluripotency networks, and functional mapping of methylation-sensitive regulatory elements in human cell models.
TET1 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient TET1 upregulation across a broader range of human cell types.
TET1 Lentiviral Activation Particles (h2) 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 TET1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TET1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TET1 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.