CAMTA1 Double Nickase Plasmid (h): sc-405328-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CAMTA1 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- CAMTA1 Double Nickase Plasmid (h) and CAMTA1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CAMTA1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CAMTA1 Double Nickase Plasmid (h) | sc-405328-NIC | 20 µg | $410.00 | |||
CAMTA1 Double Nickase Plasmid (h2) | sc-405328-NIC-2 | 20 µg | $410.00 |
CAMTA1 encodes calmodulin-binding transcription activator 1, a nuclear transcription factor that couples Ca2+/calmodulin signaling to gene expression programs. Through its CG-1 DNA-binding domain and regulatory ankyrin repeats, CAMTA1 integrates calcium-dependent cues with chromatin and transcriptional control, influencing neuronal differentiation, synaptic activity–linked transcription, and broader stress-responsive pathways. Altered CAMTA1 regulation has been associated with neurodevelopmental and neurodegenerative phenotypes, and genomic disruption of CAMTA1 is recurrently observed in several cancers, supporting its relevance to studies of transcriptional dysregulation. These attributes make CAMTA1 a useful target for dissecting calcium-driven transcriptional networks and cell state transitions in human model systems.
CAMTA1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CAMTA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CAMTA1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt CAMTA1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of CAMTA1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.