
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GHRH CRISPR Activation Plasmid (h) | sc-404753-ACT | 20 µg | $397.00 |
Human GHRH encodes growth hormone–releasing hormone, a hypothalamic peptide that stimulates anterior pituitary somatotrophs to secrete growth hormone via GHRHR engagement and downstream cAMP/PKA signaling. Through regulation of the GH–IGF axis, GHRH contributes to systemic growth, metabolic homeostasis, and neuroendocrine control of energy balance. Altered GHRH signaling has been associated with dysregulated pituitary function and abnormal growth phenotypes, and it is frequently examined in endocrine and metabolic disease research. In addition to central neuroendocrine roles, GHRH pathway activity is studied for its effects on cell proliferation and survival programs in relevant cellular models.
GHRH CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GHRH expression without altering the underlying DNA sequence.
GHRH CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GHRH 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 GHRH transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GHRH expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GHRH locus and enabling the study of GHRH-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GHRH pathway restoration in tumor cells with silenced or reduced GHRH expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.