CREM Double Nickase Plasmid (h): sc-400406-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CREM 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
- CREM Double Nickase Plasmid (h) and CREM Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CREM. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CREM Antibody (22): sc-101530
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CREM Double Nickase Plasmid (h) | sc-400406-NIC | 20 µg | $410.00 | |||
CREM Double Nickase Plasmid (h2) | sc-400406-NIC-2 | 20 µg | $410.00 |
CREM (cAMP response element modulator) is a bZIP transcription factor that binds cAMP response elements to regulate stimulus-dependent gene expression programs. In human cells it integrates cAMP/PKA signaling and interfaces with MAPK- and calcium-responsive pathways to control transcriptional outputs involved in proliferation, differentiation, metabolism, and cell survival. CREM is particularly relevant to neuroendocrine and reproductive biology, where it contributes to circadian and hormonal regulation of gene networks. Dysregulated CREM activity has been associated with altered transcriptional states reported across cancers and immune-related contexts, supporting its use as a mechanistic node for pathway-focused studies.
CREM Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CREM locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CREM. 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 CREM 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 CREM-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.