IL-3/IL-5/GM-CSFRβ CRISPR Activation Plasmid (h): sc-401045-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IL-3/IL-5/GM-CSFRβ CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IL-3/IL-5/GM-CSFRβ 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-3/IL-5/GM-CSFRβ CRISPR Activation Plasmid (h) and IL-3/IL-5/GM-CSFRβ CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CSF2RB 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-3/IL-5/GM-CSFRβ Antibody (1C1): sc-21765
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IL-3/IL-5/GM-CSFRβ CRISPR Activation Plasmid (h) | sc-401045-ACT | 20 µg | $397.00 |
CSF2RB encodes the common β subunit shared by the IL-3, IL-5, and GM-CSF receptor complexes, forming a high-affinity signaling unit with ligand-specific α chains on hematopoietic and myeloid cells. Upon cytokine engagement, IL-3/IL-5/GM-CSF receptor β initiates JAK2/STAT5 signaling and coordinates PI3K–AKT and MAPK/ERK cascades to regulate progenitor survival, proliferation, differentiation, and functional activation. This receptor node is central to cytokine-driven inflammatory and immune programs, linking bone marrow output to peripheral effector responses. Dysregulated CSF2RB signaling is studied in the context of aberrant myelopoiesis, altered leukocyte activation, and inflammatory disease mechanisms.
IL-3/IL-5/GM-CSFRβ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CSF2RB expression without altering the underlying DNA sequence.
IL-3/IL-5/GM-CSFRβ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CSF2RB 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 CSF2RB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IL-3/IL-5/GM-CSFRβ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CSF2RB locus and enabling the study of IL-3/IL-5/GM-CSFRβ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IL-3/IL-5/GM-CSFRβ pathway restoration in tumor cells with silenced or reduced CSF2RB expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.