
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD42d CRISPR Activation Plasmid (h) | sc-404793-ACT | 20 µg | $397.00 |
GP5 encodes the platelet glycoprotein V (CD42d), a component of the GPIb-IX-V receptor complex that regulates platelet adhesion and activation under high shear conditions. Through interactions with von Willebrand factor and thrombin-responsive signaling, CD42d contributes to primary hemostasis, cytoskeletal remodeling, and integrin activation that support thrombus formation. Altered abundance or function of the GPIb-IX-V complex is associated with platelet dysfunction phenotypes and bleeding or thrombotic predisposition, making GP5 a relevant node in studies of vascular biology and coagulation. In experimental systems, GP5 expression can also serve as a marker for megakaryocyte/platelet lineage programs and receptor complex assembly.
CD42d CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GP5 expression without altering the underlying DNA sequence.
CD42d CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GP5 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 GP5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD42d expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GP5 locus and enabling the study of CD42d-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD42d pathway restoration in tumor cells with silenced or reduced GP5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.