TMEM38B Lentiviral Activation Particles (h): sc-412461-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- TMEM38B 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
- TMEM38B 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 TMEM38B Lentiviral Activation Plasmid (h) and TMEM38B Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the TMEM38B promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM38B Lentiviral Activation Particles (h) | sc-412461-LAC | 200 µl | $455.00 |
TMEM38B encodes a multi-pass membrane protein of the endoplasmic reticulum that forms a cation channel implicated in regulating intracellular calcium handling. By modulating Ca2+ flux and coupling ER calcium dynamics to excitation–contraction and stress-adaptive signaling, TMEM38B can influence processes such as calcium homeostasis, ER function, and downstream transcriptional programs. Genetic disruption of TMEM38B has been linked to skeletal phenotypes, including forms of osteogenesis imperfecta, underscoring its relevance to bone biology and connective tissue integrity. These properties make TMEM38B a useful target for studying calcium-dependent signaling, ER-related pathways, and genotype–phenotype relationships in human cellular models.
TMEM38B 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 TMEM38B upregulation across a broader range of human cell types.
TMEM38B 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 TMEM38B transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TMEM38B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TMEM38B 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.