CAMTA1 CRISPR Activation Plasmid (h): sc-405328-ACT

Human CAMTA1 encodes calmodulin-binding transcription activator 1, a nuclear DNA-binding protein that integrates Ca2+/calmodulin signaling with transcriptional control. CAMTA1 participates in regulation of gene expression programs linked to neuronal differentiation, synaptic function, and cellular stress responses, consistent with its roles in chromatin-associated transcriptional regulation. Altered CAMTA1 activity has been associated with neurodevelopmental phenotypes and cerebellar dysfunction, and genomic changes affecting CAMTA1 have been reported in multiple tumor profiling studies, supporting its utility as a research target in disease-relevant transcriptional networks. These features make CAMTA1 a useful node for dissecting calcium-dependent transcriptional pathways and downstream gene regulatory circuits.

CAMTA1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CAMTA1 expression without altering the underlying DNA sequence.

CAMTA1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CAMTA1 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 CAMTA1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CAMTA1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CAMTA1 locus and enabling the study of CAMTA1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CAMTA1 pathway restoration in tumor cells with silenced or reduced CAMTA1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.