
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SRGAP1 CRISPR Activation Plasmid (h) | sc-403408-ACT | 20 µg | $397.00 |
SRGAP1 (SLIT-ROBO Rho GTPase-activating protein 1) encodes a multidomain RhoGAP that links SLIT/ROBO guidance cues to remodeling of the actin cytoskeleton. By modulating Rho family GTPases and coordinating membrane dynamics, SRGAP1 influences neurite outgrowth, neuronal migration, and synapse-associated morphology, and it participates in processes such as cell adhesion and directed motility. These functions position SRGAP1 within signaling networks that govern cytoskeletal organization and developmental patterning, with relevance to neurodevelopmental phenotypes and dysregulated cell movement in disease models.
SRGAP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SRGAP1 expression without altering the underlying DNA sequence.
SRGAP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SRGAP1 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 SRGAP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SRGAP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SRGAP1 locus and enabling the study of SRGAP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SRGAP1 pathway restoration in tumor cells with silenced or reduced SRGAP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.