IGFBP2 CRISPR Activation Plasmid (m): sc-421063-ACT

Mouse Igfbp2 encodes insulin-like growth factor binding protein 2 (IGFBP2), a secreted regulator that modulates IGF-I and IGF-II bioavailability and shapes downstream signaling through the IGF1R–PI3K/AKT and MAPK pathways. Beyond ligand sequestration, IGFBP2 can influence cell adhesion and migration via interactions with extracellular matrix components, supporting roles in tissue remodeling and developmental programs. Altered IGFBP2 expression is frequently used as a molecular readout in studies of metabolic homeostasis, inflammation, and oncogenic signaling networks, where it correlates with changes in proliferation, survival, and invasive phenotypes. These properties make Igfbp2 a valuable node for dissecting growth factor–driven pathway crosstalk in mouse disease models.

IGFBP2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Igfbp2 expression without altering the underlying DNA sequence.

IGFBP2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Igfbp2 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 Igfbp2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IGFBP2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Igfbp2 locus and enabling the study of IGFBP2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IGFBP2 pathway restoration in tumor cells with silenced or reduced Igfbp2 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.