
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Gas1 CRISPR Activation Plasmid (h) | sc-404384-ACT | 20 µg | $397.00 |
Human GAS1 (growth arrest specific 1) encodes a GPI-anchored cell surface protein that modulates morphogen signaling and cell cycle control, with prominent roles in developmental patterning and regulation of proliferation. Gas1 can influence Hedgehog pathway activity through interactions with ligands and receptors at the plasma membrane, linking extracellular cues to transcriptional programs that shape differentiation and growth arrest. Altered GAS1 expression has been associated with dysregulated Hedgehog signaling and changes in cell fate decisions, processes frequently studied in neurodevelopment, tissue homeostasis, and tumor biology. As a membrane-localized regulator, GAS1 is also relevant for investigating receptor organization, signaling thresholding, and context-dependent pathway crosstalk.
Gas1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GAS1 expression without altering the underlying DNA sequence.
Gas1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GAS1 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 GAS1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Gas1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GAS1 locus and enabling the study of Gas1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Gas1 pathway restoration in tumor cells with silenced or reduced GAS1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.