
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD42c CRISPR Activation Plasmid (h) | sc-403712-ACT | 20 µg | $397.00 |
GP1BB encodes glycoprotein Ib beta (CD42c), an essential subunit of the platelet GPIb-IX-V receptor complex that mediates adhesion of platelets to von Willebrand factor under high shear conditions. Through coordinated signaling with other complex components, CD42c supports platelet tethering, activation, and cytoskeletal rearrangements that influence thrombus formation and hemostatic responses. Disruption or altered expression of GP1BB perturbs platelet receptor surface assembly and function, linking this pathway to inherited platelet adhesion defects and abnormal bleeding phenotypes. As a result, GP1BB regulation is frequently studied in megakaryopoiesis, platelet biogenesis, and shear-dependent platelet signaling models.
CD42c CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GP1BB expression without altering the underlying DNA sequence.
CD42c CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GP1BB 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 GP1BB transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD42c expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GP1BB locus and enabling the study of CD42c-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD42c pathway restoration in tumor cells with silenced or reduced GP1BB expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.