
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CCP2 CRISPR Activation Plasmid (h) | sc-410133-ACT | 20 µg | $397.00 |
Human AGBL2 encodes cytosolic carboxypeptidase 2 (CCP2), a zinc-dependent deglutamylase that trims polyglutamate side chains on tubulin and other substrates to shape post-translational modification patterns. By regulating the balance of glutamylation, CCP2 influences microtubule stability, intracellular transport, and cilia-related processes, with downstream effects on cell division and cytoskeletal remodeling. Altered tubulin glutamylation is linked to defects in mitotic fidelity and neuronal function, and dysregulation of AGBL2 has been investigated in contexts involving aberrant proliferation and cellular stress responses. These features make CCP2 a useful node for studying the tubulin code and microtubule-driven signaling in human cells.
CCP2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous AGBL2 expression without altering the underlying DNA sequence.
CCP2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the AGBL2 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 AGBL2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CCP2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native AGBL2 locus and enabling the study of CCP2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CCP2 pathway restoration in tumor cells with silenced or reduced AGBL2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.