
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CaMKV CRISPR Activation Plasmid (h) | sc-404961-ACT | 20 µg | $397.00 |
CAMKV encodes CaMKV (Ca2+/calmodulin-dependent protein kinase-like), an atypical member of the CaMK family implicated in neuronal signaling and activity-dependent regulation of gene expression. CaMKV has been linked to calcium/calmodulin-responsive processes that influence synaptic plasticity, neurite development, and cytoskeletal dynamics, integrating upstream calcium flux with downstream transcriptional programs. Dysregulated CAMKV expression or signaling has been associated with neurodevelopmental and neuropsychiatric phenotypes, making it relevant for studying molecular mechanisms that shape neuronal connectivity and excitability. Human CAMKV is therefore a useful target for dissecting calcium-dependent pathways in neuronal models and related cellular systems.
CaMKV CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CAMKV expression without altering the underlying DNA sequence.
CaMKV CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CAMKV 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 CAMKV transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CaMKV expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CAMKV locus and enabling the study of CaMKV-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CaMKV pathway restoration in tumor cells with silenced or reduced CAMKV expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.