
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
G0S2 CRISPR Activation Plasmid (h) | sc-402335-ACT | 20 µg | $397.00 |
Human G0S2 (G0/G1 switch 2) encodes a small regulatory protein implicated in coordinating lipid metabolism and cellular quiescence. G0S2 interacts with key metabolic enzymes to modulate lipolysis and has been linked to mitochondrial function, oxidative stress responses, and transcriptional programs that shape energy homeostasis. Its expression is dynamically regulated during differentiation and inflammatory signaling, connecting G0S2 to adipocyte biology, immune cell state transitions, and broader metabolic adaptation. Dysregulated G0S2 expression has been reported across multiple disease contexts, supporting its use as a molecular handle to study pathway-level perturbations rather than direct clinical outcomes.
G0S2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous G0S2 expression without altering the underlying DNA sequence.
G0S2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the G0S2 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 G0S2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous G0S2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native G0S2 locus and enabling the study of G0S2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of G0S2 pathway restoration in tumor cells with silenced or reduced G0S2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.