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.
SEMA3G CRISPR Activation Plasmid (m): sc-432329-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SEMA3G CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SEMA3G CRISPR Activation Plasmid (m) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting 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 SEMA3G CRISPR Activation Plasmid (m) and SEMA3G CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Sema3g transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SEMA3G CRISPR Activation Plasmid (m) | sc-432329-ACT | 20 µg | $397.00 | |||
SEMA3G CRISPR Activation Plasmid (m2) | sc-432329-ACT-2 | 20 µg | $397.00 |
Sema3g encodes semaphorin 3G (SEMA3G), a secreted class 3 semaphorin that helps coordinate intercellular guidance cues affecting cell migration, adhesion, and tissue patterning. SEMA3G primarily signals through neuropilin and plexin receptor complexes to modulate cytoskeletal dynamics and downstream pathways such as Rho family GTPase signaling, thereby influencing directional motility and morphogenesis. In mouse systems, altered semaphorin signaling has been linked to dysregulated neurovascular patterning, angiogenic remodeling, and inflammatory cell trafficking, making Sema3g relevant to studies of development and disease-associated microenvironment changes. Its pathway context supports investigation of how extracellular guidance ligands reshape endothelial behavior, neuronal connectivity, and stromal organization.
SEMA3G CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Sema3g expression without altering the underlying DNA sequence.
SEMA3G CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Sema3g locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Sema3g transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SEMA3G expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Sema3g locus and enabling the study of SEMA3G-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SEMA3G pathway restoration in tumor cells with silenced or reduced Sema3g expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.