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.
IL-12B p40 CRISPR Activation Plasmid (h): sc-401407-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-12B p40 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IL-12B p40 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 IL-12B p40 CRISPR Activation Plasmid (h) and IL-12B p40 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the IL12B 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: IL-12B p40 Antibody (F-10): sc-365389
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-12B p40 CRISPR Activation Plasmid (h) | sc-401407-ACT | 20 µg | $397.00 | |||
IL-12B p40 CRISPR Activation Plasmid (h2) | sc-401407-ACT-2 | 20 µg | $397.00 |
Human IL12B encodes the p40 subunit shared by the heterodimeric cytokines IL-12 (p35/p40) and IL-23 (p19/p40), positioning IL-12B as a central regulator of innate-to-adaptive immune communication. p40-dependent signaling through IL-12R and IL-23R complexes activates JAK/STAT pathways, shaping Th1 and Th17 polarization, interferon-γ induction, and inflammatory cytokine networks in myeloid and lymphoid cells. Altered IL12B expression or pathway imbalance has been linked to dysregulated host defense and chronic inflammatory phenotypes, making it relevant to studies of infection biology, granulomatous inflammation, and cytokine-driven immune pathology. This gene is frequently interrogated in macrophage and dendritic cell activation models and in co-culture systems that measure T cell differentiation and effector function.
IL-12B p40 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IL12B expression without altering the underlying DNA sequence.
IL-12B p40 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IL12B 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 IL12B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-12B p40 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IL12B locus and enabling the study of IL-12B p40-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-12B p40 pathway restoration in tumor cells with silenced or reduced IL12B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.