IGF-1 Receptor α/β/IGF1R CRISPR Activation Plasmid (h): sc-400084-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- IGF-1 Receptor α/β/IGF1R CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- IGF-1 Receptor α/β/IGF1R 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 IGF-1 Receptor α/β/IGF1R CRISPR Activation Plasmid (h) and IGF-1 Receptor α/β/IGF1R CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the IGF1R 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: IGF-1 Receptor/IGF1R Antibody (7G11): sc-81464
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IGF-1 Receptor α/β/IGF1R CRISPR Activation Plasmid (h) | sc-400084-ACT | 20 µg | $397.00 | |||
IGF-1 Receptor α/β/IGF1R CRISPR Activation Plasmid (h2) | sc-400084-ACT-2 | 20 µg | $397.00 |
IGF1R encodes the insulin-like growth factor 1 receptor, a disulfide-linked α/β receptor tyrosine kinase that binds IGF ligands to regulate cellular growth, survival, and differentiation. Upon activation, IGF1R initiates canonical PI3K–AKT–mTOR and RAS–RAF–MEK–ERK signaling, influencing cell-cycle progression, apoptosis resistance, and metabolic programs. IGF1R crosstalk with insulin receptor signaling and integrin-mediated adhesion further shapes motility and stress responses in many tissues. Dysregulated IGF1R expression or signaling is frequently investigated in contexts of oncogenic transformation, therapy resistance phenotypes, and metabolic or developmental disorders.
IGF-1 Receptor α/β/IGF1R CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IGF1R expression without altering the underlying DNA sequence.
IGF-1 Receptor α/β/IGF1R CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IGF1R 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 IGF1R transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IGF-1 Receptor α/β/IGF1R expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IGF1R locus and enabling the study of IGF-1 Receptor α/β/IGF1R-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IGF-1 Receptor α/β/IGF1R pathway restoration in tumor cells with silenced or reduced IGF1R expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.