
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NMBR CRISPR Activation Plasmid (h) | sc-405037-ACT | 20 µg | $397.00 |
Neuromedin B receptor (NMBR) is a G protein–coupled receptor that binds the bombesin-like peptide neuromedin B to regulate intracellular calcium mobilization and downstream MAPK/ERK and phospholipase C signaling. NMBR activity influences neuroendocrine and gastrointestinal physiology, including modulation of smooth muscle contractility, secretion, and neuronal excitability. Aberrant NMBR expression and signaling have been investigated in the context of cell proliferation, migration, and receptor-driven transcriptional programs across diverse tissue types. As a surface receptor coupling extracellular ligands to second-messenger cascades, NMBR provides a tractable node for dissecting GPCR signaling dynamics and pathway crosstalk.
NMBR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NMBR expression without altering the underlying DNA sequence.
NMBR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NMBR 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 NMBR transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NMBR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NMBR locus and enabling the study of NMBR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NMBR pathway restoration in tumor cells with silenced or reduced NMBR expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.