
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Gβ 4 CRISPR Activation Plasmid (h) | sc-400820-ACT | 20 µg | $397.00 |
GNB4 encodes the human heterotrimeric G protein beta subunit Gβ 4, a core scaffold that stabilizes Gα and Gγ subunits and propagates signals downstream of activated GPCRs. By coordinating effector engagement, Gβ 4 helps modulate second-messenger pathways such as cAMP/PKA and PLCβ–IP3/DAG–Ca²⁺ signaling, influencing kinase cascades including MAPK/ERK. These processes regulate context-dependent outcomes in proliferation, differentiation, secretion, and neuronal excitability. Altered GPCR–G protein signaling dynamics involving GNB4 have been studied in relation to neurological phenotypes and broader signaling dysregulation relevant to disease-associated cellular states.
Gβ 4 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GNB4 expression without altering the underlying DNA sequence.
Gβ 4 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GNB4 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 GNB4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Gβ 4 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GNB4 locus and enabling the study of Gβ 4-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Gβ 4 pathway restoration in tumor cells with silenced or reduced GNB4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.