
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
INSM1 CRISPR Activation Plasmid (h) | sc-402424-ACT | 20 µg | $397.00 |
INSM1 (insulinoma-associated 1) encodes a zinc-finger transcription factor that functions as a key regulator of neuroendocrine differentiation and lineage maintenance. It modulates gene programs involved in cell fate specification, secretory vesicle biogenesis, and endocrine/neural transcriptional networks, integrating with pathways that control developmental timing and terminal differentiation. In human tissues, INSM1 expression is tightly restricted and is commonly used as a molecular indicator of neuroendocrine identity, reflecting its role in regulating neuroendocrine gene expression. Dysregulated INSM1-associated transcriptional programs are frequently investigated in the context of neuroendocrine tumor biology, cell state plasticity, and differentiation-dependent phenotypes.
INSM1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous INSM1 expression without altering the underlying DNA sequence.
INSM1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the INSM1 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 INSM1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous INSM1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native INSM1 locus and enabling the study of INSM1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of INSM1 pathway restoration in tumor cells with silenced or reduced INSM1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.