
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IGFBP4 CRISPR Activation Plasmid (m) | sc-421065-ACT | 20 µg | $397.00 |
Mouse Igfbp4 encodes insulin-like growth factor binding protein 4 (IGFBP4), a secreted regulator of IGF bioavailability that modulates IGF1/IGF2 signaling to influence PI3K–AKT and MAPK pathway activity. By binding IGFs and shaping receptor engagement, IGFBP4 helps govern cell growth, survival, differentiation, and tissue remodeling in multiple physiological contexts. IGFBP4 has been linked to extracellular matrix–associated processes and protease-sensitive regulation that can fine-tune local IGF signaling dynamics. Dysregulated IGF axis control involving IGFBP4 is relevant to research on developmental biology, fibrosis and wound repair, metabolic phenotypes, and tumor microenvironment signaling in mouse models.
IGFBP4 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Igfbp4 expression without altering the underlying DNA sequence.
IGFBP4 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Igfbp4 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 Igfbp4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IGFBP4 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Igfbp4 locus and enabling the study of IGFBP4-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IGFBP4 pathway restoration in tumor cells with silenced or reduced Igfbp4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.