
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CALML3 CRISPR Activation Plasmid (h) | sc-400954-ACT | 20 µg | $397.00 |
Human CALML3 (calmodulin-like 3) encodes a calcium-binding EF-hand protein that functions as a calcium sensor and modulator of calcium-dependent signaling, influencing protein–protein interactions and downstream kinase and cytoskeletal regulation. CALML3 expression is enriched in epithelial contexts and has been linked to differentiation programs, cell junction organization, and calcium-regulated remodeling processes. Through integration with broader Ca2+ signaling networks, CALML3 can impact transcriptional responses and cellular stress adaptation. Dysregulated calcium signaling and altered CALML3 expression patterns have been reported in studies of epithelial transformation and tumor biology, supporting its value as a research target in disease-relevant cell state transitions.
CALML3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CALML3 expression without altering the underlying DNA sequence.
CALML3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CALML3 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 CALML3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CALML3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CALML3 locus and enabling the study of CALML3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CALML3 pathway restoration in tumor cells with silenced or reduced CALML3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.