
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GH CRISPR Activation Plasmid (h) | sc-401112-ACT | 20 µg | $397.00 |
Human GH1 encodes growth hormone (GH), a pituitary-derived peptide hormone that regulates systemic growth, body composition, and metabolic homeostasis. GH signaling engages the GH receptor to activate JAK2/STAT5 transcriptional programs and intersects with PI3K–AKT and MAPK cascades, coordinating IGF axis activity, nutrient utilization, and anabolic processes across multiple tissues. Altered GH1 expression or disrupted GH pathway regulation is associated with growth disorders and broader endocrine-metabolic phenotypes, making GH1 a useful node for studying hormone-driven transcription, feedback control, and tissue-specific signaling responses. In cellular models, GH can influence proliferation, differentiation, and stress-response gene networks via downstream STAT-dependent and IGF-related pathways.
GH-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GH1 expression without altering the underlying DNA sequence.
GH-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GH1 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 GH1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GH-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GH1 locus and enabling the study of GH-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GH-1 pathway restoration in tumor cells with silenced or reduced GH1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.