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.
Z39Ig CRISPR Activation Plasmid (h): sc-404067-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Z39Ig CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Z39Ig CRISPR Activation Plasmid (h) 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 Z39Ig CRISPR Activation Plasmid (h) and Z39Ig CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the VSIG4 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Z39Ig Antibody (6H8): sc-53977
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Z39Ig CRISPR Activation Plasmid (h) | sc-404067-ACT | 20 µg | $397.00 | |||
Z39Ig CRISPR Activation Plasmid (h2) | sc-404067-ACT-2 | 20 µg | $397.00 |
Human VSIG4 (Z39Ig) encodes a B7 family-related immunoregulatory receptor predominantly expressed on tissue-resident macrophages, including Kupffer cells, where it modulates innate and adaptive immune crosstalk. VSIG4 functions as a complement receptor for C3 fragments and participates in phagocytic clearance and suppression of T cell activation, shaping inflammatory tone within the tissue microenvironment. Through these activities, Z39Ig influences complement-mediated opsonization, macrophage polarization programs, and immune checkpoint–like signaling that constrains excessive cytokine production. Dysregulated VSIG4 expression and macrophage-associated pathways are frequently investigated in contexts such as chronic inflammation, fibrosis, infection biology, and tumor immune evasion mechanisms.
Z39Ig CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous VSIG4 expression without altering the underlying DNA sequence.
Z39Ig CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the VSIG4 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 VSIG4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Z39Ig expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native VSIG4 locus and enabling the study of Z39Ig-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Z39Ig pathway restoration in tumor cells with silenced or reduced VSIG4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.